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Y3 Med LO's > Gastro > Flashcards

Gastro Flashcards

1
Q

How would you recognise an upper GI bleed?

A
  • Haematemesis
  • Melena
  • Raised Urea
  • Features associated with a particular diagnosis e,g,
    oesophageal varices: stigmata of chronic liver disease
    peptic ulcer disease: abdominal pain
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2
Q

How would you investigate an upper GI bleed?

A
  • FBC- clotting profile and LFTs, urea
  • Group and cross match
  • Blood glucose and ketones
  • Stool test for occult bleeding
  • Upper endoscopy
  • Colonoscopy
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3
Q

What risk assessment score is used at firs assessment of an upper GI bleed- to determine whether a patient can be an outpatient?

A

Glasgow-Blatchford

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4
Q

What risk assessment is used after endoscopy?

A

Rockall
- Provides a percentage risk of re-bleeding and mortality
- Includes age, features of shock, co-morbidities, aetiology of bleeding and endoscopic stigmata of recent hemorrhage

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5
Q

What is the guideline of endoscopy with an upper GI bleed?

A

All patients should have endoscopy within 24 hours

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6
Q

How do you manage variceal bleeding?

A

Terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e. before endoscopy)

Band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices

Transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures

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7
Q

How do you manage non-variceal bleeding with endoscopy?

A

Adrenaline (epinephrine) should not be used as monotherapy for the endoscopic treatment of non-variceal UGIB. For the endoscopic treatment of non-variceal UGIB, one of the following should be used:

A mechanical method (eg, clips) with or without adrenaline (epinephrine).

Thermal coagulation with adrenaline (epinephrine).
Fibrin or thrombin with adrenaline (epinephrine).

Interventional radiology - should be offered to unstable patients who re-bleed after endoscopic treatment.

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8
Q

What is the acute management of an upper gastro-intestinal bleed?

A
  1. Protect the airway and give high-flow oxygen
  2. FBC, U&E, LFTs, Clotting and cross-match
  3. Give IV fluids
  4. Catheter
  5. ECG, ABG and CXR
  6. Arrange an urgent endoscopy
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9
Q

When should you give a PPI in an upper GI bleed?

A

AFTER endoscopy

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10
Q

What are key symptoms/features that are shared between Ulcerative Colitis and Crohn’s disease?

A
  • Diarrhoea
  • Arthritis
  • Erythema nodosum
  • Pyoderma gangrenosum
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11
Q

What are key symptoms/features that are significant to Ulcerative colitis?

A
  • Bloody diarrhoea
  • Primary sclerosing cholangitis
  • Uveitis
  • Tenesmus
  • Colorectal cancer
  • lleocaecal valve involvement, continuous disease
  • Crypt abscesses
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12
Q

What are key symptoms/features that are significant to Crohn’s?

A
  • Weight loss
  • Abdominal pain
  • Bowel obstruction
  • Gall stones
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13
Q

What are signs you see on endoscopy of Crohn’s?

A

Cobble-stone, deep ulcers and skip lesions

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14
Q

What are signs you see on radiology of Crohn’s?

A
  • High sensitivity and specificity for examination of the terminal ileum
  • Strictures: ‘Kantor’s string sign’
    proximal bowel dilation
  • ‘rose thorn’ ulcers
  • fistulae
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15
Q

What are signs you see on endoscopy of Ulcerative Colitis?

A

Pseudopolyps

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16
Q

What are signs you see of radiology of Ulcerative colitis?

A
  • Loss of haustrations
  • Pseudopolyps
  • Drainpipe colon
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17
Q

How is ulcerative colitis usually diagnosed?

A

Colonoscopy and biopsy

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18
Q

What antigen helps distinguish between IBD and IBS?

A

Fecal calprotectin

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19
Q

How do you investigate Ulcerative colitis and Crohn’s?

A
  • FBC
  • LFTs - hypoalbuminaemia
  • Stool MC&S to exclude infection
  • Iron studies
  • CRP/ESR
  • Colonoscopy and biopsy
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20
Q

What assessment tool is used in ulcerative colitis?

A

True love and witt’s

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21
Q

What is mild ulcerative colitis defined as?

A

< 4 stools/day, only a small amount of blood

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22
Q

What is moderate ulcerative colitis defined as?

A

4-6 stools/day, varying amounts of blood, no systemic upset

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23
Q

What is severe ulcerative colitis defined as?

A

> 6 stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)

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24
Q

How do you induce remission in severe colitis?

A
  • Intravenous steroids
  • Intravenous ciclosporin if steroid use is contraindicated
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25
Q

How do you treat mild-moderate proctitis?

A

Rectal mesalazine
If remission not achieved within 4 weeks, add an oral aminosalicyclate
IF still not achieved- add topical or oral corticosteroid

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26
Q

How do you treat mild-moderate proctosigmoiditis and left-sided ulcerative colitis?

A

Rectal mesalazine
If remission not achieved in 4 weeks,
Add high dose oral mesalazine or
Switch to a high dose oral mesalazine and a topical corticosteroid

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27
Q

How do you treat extensive disease in mild-moderate ulcerative colitis?

A

Rectal mesalazine and high dose mesalazine
If not achieved within 4 weeks, stop topical treatments and offer a high dose mesalazine and oral corticosteroid.

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28
Q

What is the medical management to maintain remission in Crohn’s?

A

Azathioprine or mercaptopurine

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29
Q

How do you induce remission in Crohn’s?

A
  • Glucocorticoids (oral, topical or intravenous) Prednisolone or IV hydrocortisone
  • Mesalazine if glucocorticoids are not effective
  • Azathioprine or mercaptopurine as an add-on
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30
Q

What are some clinical features of malnutrition?

A
  • High susceptibility or long durations of infections
  • Slow or poor wound healing
  • Altered vital signs including bradycardia, hypotension and hypothermia
  • Depleted subcutaneous fat
  • Low skeletal muscle mass
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31
Q

What are some complications of refeeding syndrome?

A

Potassium and phosphate become depleted when there is a surge in insulin response

Results in hypokalaemia and hypophosphataemia- can result in cardiac complications (arrhythmias) and seizures

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32
Q

What is the cause of Kwashiorkor?

A

Low protein intake can result in insufficient blood protein synthesis leading to a decrease in plasma oncotic pressure and oedema.

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33
Q

What are some screening tools for malnutrition?

A

MUST
MNA (mini nutritional assessment form)

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34
Q

How do you investigate malnutriiton?

A
  • Height and weight (severe malnutrition is defined as the wight for height z score more than three sd.s below the mean)
  • BMI
  • Mid upper arm diameter
  • Skin folds

Blood glucose
FBC and film
Urine MC&S
Stool OC&P
Serum albumin
HIV test
U&Es
Iron studies, folate, B12.
Pre-albumin, transferrin, retinol-binding protein (better short-term indicators of protein status than albumin alone).
TFTs.
Coeliac serology.
Calcium, phosphate, zinc.
Vitamin levels - if deficiency is suspected.

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35
Q

How do you manage malnutrition?

A

Management of malnutrition is difficult. NICE recommend the following points:
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

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36
Q

What are the most common causes of acute liver failure?

A

Paracetamol overdose
Alcohol
Viral hepatitis (usually A or B)
Acute fatty liver of pregnancy

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37
Q

How is ALF identified?

A

ALF is characterised by the presence of coagulopathy (INR > 1.5) and HE. This is usually accompanied by transaminitis (i.e. deranged liver function tests ALT/AST) and hyperbilirubinaemia. ALF is usually initiated following a severe acute liver injury (ALI)

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38
Q

How can the severity of hepatic encephalopathy be determined?

A

Using the west haven criteria

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39
Q

What are some signs and symptoms of acute liver failure?

A

Altered mental status
Confusion
Asterixis: flapping tremor suggestive of HE
Jaundice
Right upper quadrant pain (variable)
Hepatomegaly
Ascites
Bruising (coagulopathy)
GI bleeding: haematemesis, melaena
Hypotension and tachycardia: reduce systemic vascular resistance and hyperdynamic circulation
Raised intracranial pressure: papilloedema, bradycardia, hypertension, low GCS

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40
Q

Is an emergency liver transplantation an option for primary or secondary causes of ALF?

A

Both

Primary is

Primary causes:
Viruses (A, B, E)
Paracetamol
Non-paracetamol medications (e.g. Statins, Carbamazepine, Ecstasy)
Toxin-induced (e.g. Amanita phalloides - death cap mushroom that contains amatoxins and phallotoxins)
Budd-chiari syndrome
Pregnancy-related (e.g. fatty liver of pregnancy, HELLP syndrome)
Autoimmune hepatitis
Wilson’s disease

Secondary
Ischaemic hepatitis
Liver resection (post-hepatectomy liver failure)
Severe infection (e.g. malaria)
Malignant infiltration (e.g. lymphoma)
Heat stroke
Haemophagocytic syndromes

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41
Q
A
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41
Q

What are some urgent blood tests that are needed when you suspect ALF?

A

Full blood count
Urea & electrolytes
Liver function tests: including conjugated and unconjugated bilirubin
Bone profile
Blood glucose
Arterial ammonia
Arterial blood gas (pH and lactate)
Coagulation: urgent INR
Lactate dehydrogenase
Lipase/amylase: pancreatitis complication of ALF
Blood cultures: sepsis is major cause of morbidity and mortality

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42
Q

What are three things that are needed in ALF to referral to a liver transplant?

A
  • Formal clinical assessment
  • Urgent blood tests
  • Non-invasive liver screen
  • Imaging
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43
Q

What is essential imaging in diagnosing ALF?

A

Ultrasound

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44
Q

What is the key difference between acute liver injury and acute liver failure?

A

Hepatic encephalopathy

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45
Q

What makes up a non-invasive liver screen?

A

Toxicology screen: serum/urine
Paracetamol serum level
Autoimmune markers: ANA, autoantibodies, immunoglobulins, ANCA
Viral screen:
Hepatitis A: anti-HAV IgM
Hepatitis B: HBsAg, anti-HBc IgM +/- HBV DNA levels
Hepatitis C: anti-HCV (unlikely to cause ALF - may be co-infected)
Hepatitis D: if positive for HBV
Hepatitis E: anti-HEV IgM +/- HEV RNA levels
Other: CMV, EBV, HSV, VZV, Parvovirus

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46
Q

What are some contraindications to a liver transplant?

A
  • Previous cirrhosis
  • Heavy alcohol use
  • Major cardiac or respiratory disease
  • Terminal illness
47
Q

What is the king’s college criteria for a liver transplant for paracetamol ALF?

A

Paracetamol

Arterial pH: < 7.3 after resuscitation and > 24 h since ingestion
Lactate: > 3 mmol/L after resuscitation, OR
The 3 following criteria:
Hepatic encephalopathy ≥ grade 3
Serum creatinine > 300 umol/L
INR > 6.5

48
Q

What is the king’s college criteria for a liver transplant for non-paracetamol ALF?

A

Non-paracetamol
INR: > 6.5, OR
3 out of 5 following criteria:
Aetiology: indeterminate aetiology hepatitis, drug-induced hepatitis
Age: < 10 years or > 40 years
Jaundice: Interval jaundice-encephalopathy > 7 days
Bilirubin: > 300 umol/L
INR: > 3.5

49
Q

How would you recognise a paracetamol overdose?

A
  • Nausea and vomiting
  • Mild/moderate abdominal pain/tenderness
  • Jaundice
  • Metabolic acidosis
  • Coma
  • Hepatic encephalopathy
  • Bruising or systemic hemorrhage
50
Q

What is a staggered overdose?

A

An overdose is considered staggered if all the tablets were not taken within 1 hour.

51
Q

What is the therapeutic dose of paracetamol in adults?

A

1g four times a day with a maximum of 4g per day.

52
Q

What g of paracetamol is potentially fatal?

A

12

53
Q

What dose of paracetamol is associated with serious or fatal adverse effects from toxicity?

A

> 150mg/kg

54
Q

What are the 4 circumstances in which acetylcysteine should be given?

A
  1. if the amount of paracetamol (acetaminophen) in the blood is at or above a specific level at certain times (100 mg/L at 4 hours and 15 mg/L at 15 hours), it indicates a potential risk of liver damage
  2. There is a staggered overdose* or there is doubt over the time of paracetamol ingestion, regardless of the plasma paracetamol concentration; or
  3. Patients who present 8-24 hours after ingestion of an acute overdose of more than 150 mg/kg of paracetamol even if the plasma-paracetamol concentration is not yet available
  4. Patients who present > 24 hours if they are clearly jaundiced or have hepatic tenderness, their ALT is above the upper limit of normal
    acetylcysteine should be continued if the paracetamol concentration or ALT remains elevated whilst seeking specialist advice
55
Q

What are some causes of chronic liver disease?

A
  • Alcohol
  • Hepatitis
  • Inherited (wilson’s, alpha-1-antitrypsin, hemochromatosis)
  • Metabolic
  • Biliary
  • Vascular (ischaemic hepatitis, budd-chiari, congestive hepatopathy)
  • Drug induced
56
Q

How do you assess the severity of chronic liver disease?

A

Child-Pugh score

  • Encephalopathy
  • Ascites
  • Bilirubin
  • Albumin
  • INR
57
Q

How do you diagnose chronic liver disease?

A
  • LFTs
  • Transient elastography
  • USS
  • CT
  • MRI
  • Liver biopsy (gold standard)
58
Q

What is the gold standard diagnostic method for the identification of cirrhosis?

A

Liver biopsy

59
Q

When is liver transplantation considered, and what mnemonic can you use to remember it?

A

Liver transplantation is generally considered when there are features of decompensated liver disease. The four key features can be remembered with the “AHOY” mnemonic:

A – Ascites
H – Hepatic encephalopathy
O – Oesophageal varices bleeding
Y – Yellow (jaundice)

The UKELD is based on serum creatinine, sodium, bilirubin and INR. The minimum criteria for listing a patient for liver transplantation is a score ≥ 49, which represents a 9% one-year mortality without a transplant.

60
Q

Describe the management of alcoholic liver disease?

A
  • Stop drinking alcohol permanently
  • Psychological interventions (e.g., motivational interviewing or CBT)
  • Nutritional support with vitamins (particularly thiamine – vitamin B1) and a high-protein diet
  • Corticosteroids may be considered to reduce inflammation in severe alcoholic hepatitis to improve short-term outcomes (but not long-term outcomes)
  • Treat complications of cirrhosis (e.g., portal hypertension, varices, ascites and hepatocellular carcinoma)
  • Liver transplant in severe disease (generally 6 months of abstinence is required)
61
Q

What are the 4 stages of non-alcoholic fatty liver disease?

A
  1. Non-alcoholic fatty liver disease
  2. Non-alcoholic steatohepatitis
  3. Fibrosis
  4. Cirrhosis
62
Q

What are some investigations for NAFLD?

A

-Raised ALT is normally the first indication
- Liver ultrasound to diagnose hepatic steatosis (increased echogenicity)
- FIB4 or NAFLD fibrosis score
- Fibroscan
- Liver biopsy

63
Q

What is the gold standard for diagnosing NAFLD?

A
  • Fatty changes on a liver ultrasound
  • Enhanced liver fibrosis blood test
64
Q

What is a FIB-4 score used in the diagnosis of NAFLD?

A

Fibrosis 4 (FIB-4) score is another option for assessing liver fibrosis in NAFLD. It is based on an algorithm of age, liver enzymes (AST and ALT) and platelet count.

65
Q

How do you manage NAFLD?

A
  • Weight loss
  • Healthy diet (Mediterranean diet is recommended)
  • Exercise
  • Avoid/limit alcohol intake
  • Stop smoking
  • Control of diabetes, blood pressure and cholesterol
  • Refer patients where scoring tests indicate liver fibrosis to a liver specialist
  • Specialist management may include vitamin E, pioglitazone, bariatric surgery and liver transplantation
66
Q

Easy way to remember viral hepatitis?

A

Certainly! A popular and easy way to remember the hepatitis viruses is to use the mnemonic “HAV-HeBeHec-HepHe”:

HAV - Hepatitis A Virus:

Think of “A” as in “Apple” for Hepatitis A. It is often associated with contaminated food and water.
HeB - Hepatitis B Virus:

The “B” can be linked to “Be,” like a bee. Hepatitis B is commonly transmitted through blood and bodily fluids.
HeC - Hepatitis C Virus:

The “C” can be linked to “See.” Hepatitis C is often asymptomatic, and people may not “see” the symptoms for a long time.
HepHe - Hepatitis D and E:

“Hep” can be a reminder for both Hepatitis D and E.
Hepatitis D (HDV) is dependent on Hepatitis B for replication.
Hepatitis E (HEV) is often associated with contaminated water, similar to Hepatitis A.

67
Q

How do you diagnose hepatitis A?

A

Hepatitis A IgM and Hepatitis A IgG antibodies (HAV-IgM, HAV-IgG) may be used to diagnose the infection.

68
Q

Which strain of hepatitis is the only one you can cure?

A

Hepatitis C

69
Q

What is the relationship between Hepatitis D and Hepatitis B?

A

Hepatitis D can only be transmitted to patients infected with Hepatitis B.

70
Q

What are some presenting features of Haemochromatosis?

A
  • early symptoms include fatigue, erectile dysfunction and arthralgia (often of the hands)
  • ‘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)
    arthritis (especially of the hands)
71
Q

What is considered the most useful investigation marker in haemochromatosis?

A

Transferrin saturation

72
Q

Outline investigations for haemochromatosis

A
  • Liver function tests
  • Molecular genetic testing for the C282Y and H63D mutations
    MRI is generally used to quantify liver and/or cardiac iron
  • Liver biopsy is now generally only used if suspected hepatic cirrhosis
73
Q

Outline management for hemochromatosis

A

Venesection is the first-line treatment
monitoring adequacy of venesection: transferrin saturation should be kept below 50% and the serum ferritin concentration below 50 ug/l

Desferrioxamine may be used second-line (works by chelating the iron)

74
Q

Outline the difference between type 1 and type 2 autoimmune hepatitis

A

Type 1 typically affects women in their late forties or fifties. It presents around or after menopause with fatigue and features of liver disease on examination. It takes a less acute course than type 2.

Type 2 usually affects children or young people, more commonly girls. It presents with acute hepatitis with high transaminases and jaundice.

75
Q

Outline investigations of autoimmune hepatitis 1

A

Investigations will show high transaminases (ALT and AST) and minimal change in ALP levels (a “hepatitic” picture). Raised immunoglobulin G (IgG) levels are an important finding.

Autoantibodies in type 1 autoimmune hepatitis are:

Anti-nuclear antibodies (ANA)
Anti-smooth muscle antibodies (anti-actin)
Anti-soluble liver antigen (anti-SLA/LP)

76
Q

Outline investigations for autoimmune hepatitis 2

A

Investigations will show high transaminases (ALT and AST) and minimal change in ALP levels (a “hepatitic” picture). Raised immunoglobulin G (IgG) levels are an important finding.

Autoantibodies in type 2 autoimmune hepatitis are:

Anti-liver kidney microsomes-1 (anti-LKM1)
Anti-liver cytosol antigen type 1 (anti-LC1)

77
Q

What is the management of autoimmune hepatitis?

A

Treatment is with high-dose steroids (e.g., prednisolone). Other immunosuppressants are also used, particularly azathioprine. Immunosuppressant treatment is usually successful at inducing remission (controlling the disease).

Liver transplant may be required in end-stage liver disease. Autoimmune hepatitis can reoccur in the new liver

78
Q

What are some complications of chronic liver disease?

A

Hepatic encephalopathy
Ascites
Hyponatraemia
Gastrointestinal bleeding (i.e. variceal bleed)
Bacterial infections (i.e. SBP)
Acute kidney injury
Hepatocellular carcinoma
Hepatorenal syndrome
Hepatopulmonary syndrome
Acute-on-chronic liver failure

79
Q

How do you diagnose and assess the severity of esophageal varices in a patient with chronic liver disease?

A

Endoscopy is the gold standard for diagnosing esophageal varices. The severity is graded based on size, red wale marks, and the presence of cherry-red spots.

80
Q

In the context of chronic liver disease, what is hepatorenal syndrome, and how is it managed?

A

Hepatorenal syndrome is a type of functional renal failure. Management involves addressing the underlying liver disease, along with vasoconstrictors like terlipressin and albumin infusion.

81
Q

What laboratory tests are useful in assessing the degree of liver dysfunction in patients with chronic liver disease?

A

The Model for End-Stage Liver Disease (MELD) score, incorporating serum bilirubin, creatinine, and INR, provides a quantitative measure of liver dysfunction and aids in predicting prognosis.

82
Q

Discuss the role of imaging in identifying complications of chronic liver disease, specifically related to ascites.

A

Abdominal ultrasound is essential for detecting ascites, while paracentesis can be performed to analyze ascitic fluid for cell count, protein, and cultures to guide management.

83
Q

What are the two types of gallstones?

A

Cholesterol stones- imbalance bile composition, heavier patients
Super sick patients- pigment stones, too much bilirubin

84
Q

Investigations for biliary colic

A

Bedside
- Pregnancy test
- Urine dip
- Obs

Bloods
- FBC
- Us&Es
- LFTs

Imaging
- Ultrasound
- MRCP (gold standard)

85
Q

Management of gallstones

A
  • Sound wave therapy
  • Routine lap chole
  • Low fat diet
  • Spontaneous resolution
86
Q

What causes acute cholecystitis?

A
  • Blocked cystic duct
  • ERCP (foreign body)
87
Q

Inx for acute chole

A
  • US- presence of gallstones in GB
  • Gall bladder wall thickening
  • No CBD dilation
  • Murphy’s sign
  • If in doubt- MRCP
88
Q

How do you treat acute cholecystitis?

A
  • Antibiotics
  • Cholecystostomy (drain infected bile)
  • Spontaneous resolution
  • Co-Amoxiclav and taz
89
Q

Reynold’s pentad for ascending cholangitis

A
  • Fever
  • Jaundice
  • Shock
  • RUQ pain
  • Confusion
90
Q

Charcot’s triad

A
  • RUQ pain
  • Jaundice
  • Fever
91
Q

How would you treat ascending cholangitis?

A
  1. Antibiotics/NBM/IV fluids/Blood cultures
  2. Ultrasound
  3. MRCP
  4. ERCP
92
Q

Should you make patients NBM for ascending cholangitis?

A

Yes

93
Q

I GET SMASHED

A

Idiopathic
Gallstones
Ethanol
Trauma

Steroid use
Mumps
Autoimmune
Scorpion stings
Hypercalcaemia + high fats
ERCP
Drugs

94
Q

Inx for pancreatitis

A
  • Amylase (In acute pancreatitis, serum amylase activities begin to rise within 3-6 hours and normally reach a maximum after 20-30 hours.) bloods- raised inflammatory markers
  • US- presence of gallstones in GB
  • Gall bladder wall thickening
95
Q

What is the treatment of pancreatitis?

A
  • Antibiotics
  • IV fluids
  • Catheter
  • Treatment of gallstones
96
Q

How do NSAIDs cause peptic ulcer formation?

A

NSAIDs can cause peptic ulcer formation by their action in inhibiting prostaglandin synthesis, resulting in a reduced secretion of glycoprotein, mucous, and phospholipids by the gastric epithelial cells, which would otherwise normally protect the gastric mucosa

97
Q

What are the two most common causes of acute pancreatitis?

A

Gallstones and alcohol

98
Q

What are three differential diagnoses of a groin lump?

A
  • Lymphadenopathy
  • Femoral artery aneurysm
  • Saphena varix
  • Lipoma
99
Q

How can you definitively diagnose autoimmune hepatitis?

A

With a liver biopsy
A diagnosis cannot be made without histology report.

Histology will show interface hepatitis and plasma cell infiltration

100
Q

What should you measure before you start Azathioprine?

A

TPMT levels

101
Q

What will a liver biopsy for autoimmune hepatitis help us rule out?

A

This will give us a good baseline assessment of the liver, assess for presence or absence of sinister features like extensive necrosis, advanced fibrosis, cirrhosis and presence and absence of plasma cells

102
Q

How do you initially treat autoimmune hepatitis

A

High dose of steroids
Then introduce azathioprine

103
Q

How long do you treat autoimmune hepatitis for?

A

The duration of therapy in AIH is a contentious issue but most hepatologists would treat for at least two years after blood tests have normalised before discontinuing therapy. The need to perform a liver biopsy before stopping therapy is also debated but current UK guidelines recommend this. If treatment is stopped before two years almost all patients will relapse. The majority of patients will also still relapse after stopping treatment after two years. In certain situations one may even consider life long therapy e.g. for those who have cirrhosis, severe initial presentation, and prior relapse.

104
Q

What should the pH be for nasogastric tube testing?

A

1-5.5

105
Q

How would you treat a peptic stricture?

A

Balloon dilatation
PPIs

106
Q

Why would you use a flexible sigmoidoscopy in extensive disease?

A

Increased risk of perforation
Examines only lower colon, not the entire colon.
Shorter and simpler procedure.
Requires less bowel preparation.
Uses smaller and more flexible instruments.
Needs less air, reducing pressure risks.

107
Q

What are extra-intestinal features of ulcerative colitis that are related to the activity of the bowel?

A

Erythema nodosum: Skin condition that often flares up during active colitis and improves during remission.

Aphthous ulcers: Mouth ulcers that are more likely to appear or worsen during active colitis.

Episcleritis: Eye inflammation that can correlate with colitis activity.

Anterior uveitis: Another form of eye inflammation that is associated with active colitis.

Acute arthropathy: Joint pain and swelling that can flare up with colitis activity.

108
Q

When is Azathioprine recommended for management of ulcerative colitis?

A

Azathioprine is recommended for patients who are steroid-dependent or who have had 2 relapses requiring steroids or where remission is not maintained on 5-ASA agents.

109
Q

If you are suspecting IBS, what investigation should you carry out to rule out another differential?

A

Tissue Transglutaminase antibodies to rule out coeliac disease

110
Q

Give me 5 NSAIDs in increasing strength

A

Ibuprofen: Mild to moderate pain.
Naproxen: Moderate pain.
Diclofenac: Moderate to severe pain.
Indomethacin: Severe pain, anti-inflammatory.
Ketorolac: Very severe pain, short-term use.

111
Q

What does prostaglandin E do?

A

Increases mucus and bicarbonate secretion which protects the stomach lining

112
Q

What do you give if a patient is septic with C.diff?

A

Intravenous Metronidazole + oral Vancomycin

113
Q

What are common drugs that cause cholestasis?

A

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

114
Q

How do PPI’s cause hyponatremia?

A

PPIs can cause hyponatraemia by increasing ADH activity, which makes the kidneys retain more water and dilute the sodium in the blood.

Y3 Med LO's (9 decks)

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