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General Medicine > GI > Flashcards

GI Flashcards

1
Q

Convert 50mg codeine to oral morphine

A

5mg oramorph

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2
Q

Convert 30mg oramorph to syringe driver equivalent

A

15mg (divide by 2)

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3
Q

What are the 5 end of life symptoms?

A 
Pain - morphine 
SOB - morphine
Respiratory secretions- hyosceine butylbromide
Agitation- modazolam
Nausea - levomepromazine
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4
Q

Convert 20mg oramorph to diamorphine

A

10mg

Diamorphine is twice as potent

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5
Q

Young lady with sudden onset abdo pain, ascites and widely deranged LFTs. Caudate lobe is enlarged. Most likely diagnosis?

A

Budd-Chairi syndrome -

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6
Q

What is proctitis?

A

UC which affects just the rectum

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7
Q

Name 6 extra-intestinal effects of UC

A

1) Oral ulceration
2) Uveitis
3) Joint involvement
4) Skin involvement = erythema nodosum, pyoderma nodosum
5) PSC
6) Clubbing

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8
Q

In an acute attacks of UC how do you assess severity?

A

Markers:

1) No of motions/ day
2) Bleeding
3) Heart rate
4) ESR/ CRP
5) Temperature
6) Hb

E.g. in a severe acute attack there will be >6 motions/ day and the patient will have a fever, be tachycardia, anaemic and have high inflammatory markers

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9
Q

In patients who are immunosupressed long term - which cancers are they at risk of ?

A

Skin (SCC)

LYMPHOMA

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10
Q

What are the complications of UC?

A

ACUTE:

1) Perforation
2) Bleeding
3) Toxic megacolon
4) Venous thrombosis

Long term:

1) Colon cancer - colonoscopies done every 2-4 weeks.

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11
Q

First line treatment of new mild UC

A

5-ASA e.g. sulfasalazine, mezalazine

There is a risk of blood disorders e.g. agranulocytosis

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12
Q

Treatment of patient with moderate UC

A

Use steroids to try and induce remission

E.g. oral prednisolone

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13
Q

Management of severe UC e.g. >6 motions/ day and systemically unwell

A

1) Admit, NBM, IV fluids
2) Hydrocortisone 100mg/6h IV
3) Rectal steroids
4) Monitor closely e.g. pulse, T, re-examine to look for signs of perforation
5) Daily bloods
6) Consider blood transfusion if needed

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14
Q

Patient with UC attack - still frequent stools + CRP> 45 on day 3 of admission. What do you do?

A

Rescue therapy —> either infliximab or ciclosporin

This can save the bowel

Infliximab is a monoclonal antibody - anti- TNF

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15
Q

What are the side effects of infliximab and other anti-TNF drugs e.g. adalimumab

A

Infection
Reactivation of TB
Psoriasis
New onset vitiligo

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16
Q

What are the indications for a colcetomy or other surgical intervention in Crohn’s?

A

Toxic megacolon - small bowel >6cm
Massive haemorrhage
Perforation
Failed medical therapy

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17
Q

Patients with UC refractory to steroids may need immunosupression with agents such as azathioprine/ methotrexate. What must be considered before prescribing azathioprine?

A

Measure TMPT level as if levels are low, patients are at increased risk of bone marrow toxicity. Dose should be lowered or another agent used

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18
Q

Which drug is typically used for maintenance therapy is UC?

A

5-ASA e.g. sulfasalizine or mesalazine

Remember there is a risk of blood disorder- check FBC and U&E
Also sulfasalizne causes oligozoospermia

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19
Q

Which mutation is associated with Crohn’s?

A

NOD 2/ CARD 15

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20
Q

Extraintestinal features of Crohn’s?

A

1) Oral ulcers
2) Episcleritis/ iritis
3) Skin e.g. erythema nodosum
4) Arthritis
5) Anal disease e.g. skin tags, figures, peri-anal abscess

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21
Q

Complications of Crohn’s disease?

A

1) Small bowel obstruction - adhesions
2) Abscesses
3) Fistula - bladder, skin, vagina
4) perforation

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22
Q

Crohn’s likes the terminal ileum. How is this region imaged?

A

Small bowel enema or MRI small bowel

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23
Q

Transmural inflammation with cobblestoning, rose thrown ulcers and colonic strictures

A

Crohn’s disease

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24
Q

Mucosal inflammation with crypt abscess

A

Description of UC. Continuous lesions

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25
Q

Management of a mild attack of Crohns’

A

Oral prednisolone

30mg/d PO for 1 week then 20mg/d for 4 weeks then reduce by 5mg gradually if symptoms resolved

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26
Q

Management of severe Crohns flare

A

1) Admit, NBM and IV fluids
2) IV steroids e.g. hydrocortisone 100mg
3) IV metronidazole - very good for perianal disease
4) Consider blood transfusion
5) Regular assessment and examination

5 day is the key point - improving = switch to oral, not improving = infliximab/ adalimumab

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27
Q

What is the role of azathioprine in Crohn’s disease?

A

Largely for steroid sparing

Also used for triple therapy which is very effective - steroids + infliximab + azathioprine

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28
Q

Indications for surgery in Crohns

A

1) Stricture causing obstruction
2) Perforation
3) Medication failure
4) Fistulae
5) Abscesses

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29
Q

Give 5 causes of liver failure

A

1) Infection - hepatitis
2) Alcohol
3) Toxins - paracetemol
4) Vascualr - trauma/ bud Chiarri
5) Autoimmune
6) Other syndromes e.g. haemochromatosis etc

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30
Q

In patients with liver failure, hypoglycaemia is a big risk

A

Give 10% glucose IV 1L/2h and measure BM regularly

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31
Q

Remember that warfarin effects are increased by liver failure

A

Avoid hepatotoxic drugs such as paracetemol and methotrexate when prescribing in liver failure

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32
Q

What causes hepatic encephalopathy?

A

Liver fails to clear nitrogenous waste. The ammonia builds up and is taken up by brain cells (astrocytes) which converts glutamate to glutamine —> excess glutamine changes fluid balance —> cerebral oedema

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33
Q

Indications for transplant after paracetemol induced liver failure?

A

Arterial pH <7.3, 24 hours after ingestion

OR

Raised prothrombin time (PT)
Creatinine >300
Grade 3/4 encephalopathy

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34
Q

List 5 causes of liver cirrhosis

A 
Chronic alcohol abuse
Chronic HBV/ HCV
Haemochromatosis
Autoimmune disease e.g. primary sclerosing cholangitis 
Hepatic vein event e.g. Budd chairing
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35
Q

Leuconycia

A

White nails due to hypoalbuminaemia (usually chronic liver disease)

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36
Q

Advice for alcohol consumption

A

Aim for <14 units/ week
Spread over several days
With a 1-2 alcohol free days/ week

E.g 1 bottle of wine = 10 units
1 pint = 2.5 units

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37
Q

List 4 acute effects of alcohol excess

A

1) CNS impairment —> alcohol and violence
2) Oesophagitis
3) Acute oesophagitis
4) Respiratory depression/ aspiration

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38
Q

Discuss the progression of alcoholic liver disease

A

Fatty changes —> fibrosis —> cirrhosis —> hepatocellular carcinoma

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39
Q

List some signs of chronic liver disease

A 
Spider naevi
Encephalopathy
Hypoalbuminaemia 
Prolonged PT
Portal hypertension
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40
Q

What is the portal hypertension? What are the signs?

A

1) Increased pressure (>10mmHg) in the hepatic portal vein
2) Most commonly caused by cirrhosis although tumours, hepatitis and Budd-Chiari are other causes
3) The increased pressure opens up collateral vessels - the portal and systemic circulation are now connected
4) Varcies, caput medusae (umbilicus), haemorrhoids
5) Hypersplensim is common

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41
Q

The Child’s Pugh score is used to classify cirrhosis. What are the components?

A

1) Ascites
2) Encephalopathy
3) Albumin level
4) Prothrombin time
5) Bilirubin level

A score of 10-15 is decompensated cirrhosis

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42
Q

Ascites results from peripheral arterial vasodilatation and portal hypertension. Na and water retention as well as hypoalbuminaemia is also important. List 4 causes:

A

Liver cirrhosis
Malignancy e.g. GI tract/ ovarian
Heart failure
Nephrotic syndrome

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43
Q

What is the commonest liver disease?

A

NAFLD

Treatment is diet and exercise but this rarely happens

44
Q

Most likely diagnosis in a 40 year old lay presenting with fatigue, itch without rash and xanthelasma. How do you confirm?

A

PBC
Primary biliary cholangitis

AMA- anti-mitochondrial antibodies
Cholestatic LFT - alk phos and GGT are very raised
Liver biopsy

45
Q

What is the treatment for PBC?

A

DIgnsose primary biliary cholangitis using +ve AMA, LFTs and liver biopsy

Treat with ursodeoxycholic acid
Progression to liver failure and transplant is relatively common

46
Q

Piecemeal necrosis and lobular involvement on liver biopsy with interface hepatitis

A

Autoimmune hepatitis

47
Q

Which autoantibodies are associated with type 1 auto-immune hepatitis?

A

Anti-smooth muscles
Anti- nuclear

Remember typically presents as per viral hepatitis

Usually associated with other conditions e.g. autoimmune thyroiditis, Graves’ disease etc

Measure IgG and do liver biopsy

48
Q

Which autoantibodies are associated with type 2 autoimmune hepatitis?

A

Anti-liver kidney microsomal 1 (LKM-1)

Remember typically presents as per viral hepatitis

49
Q

What is the treatment of autoimmune hepatitis?

A

Corticosteroids + azathioprine

Serious condition - 40% will develop cirrhosis and 50% will develop oesophageal varices in 2 years

50
Q

40% of patients with primary sclerosing cholangitis have UC

A

Aim is to maintain bile flow and monitor risk of cholangiocarcinoma/ colo-rectal cancer

ERCP/ MRCP is used to image bile ducts +/- insert stents

51
Q

What is the differential for malabsorption?

A
  • Coeliac
  • CF
  • Crohn’s
  • Short bowel
  • tropical sprue
  • chronic pancreatitis
52
Q

What is a SeHCAT scan?

A

A radionucloetide scan which tests for bile acid malabsorption

53
Q

Features of Whipple’s disease?

A
  • diarrhoea and steatorrhoea
  • mild fever
  • polyarthralgia
  • hyperpigmentation
  • generalised lymphadenopathy
  • CNS signs

Remember it is a really rare condition caused by tropheryma whipplei

Long term ABx are the mainstay of treatment

54
Q

H. Pylori is associated with 90% duodenal ulcers

GI bleed, perforation and gastric outlet obstruction are all complications of peptic ulcer disease

A

H.pylori associated with 75% gastric ulcers

55
Q

Other than blood tests such as FBC, which other tests are used in the diagnosis of tropical sprue?

A

1) 72 hour stool collection on prescribed diet (—> assesses fat absorption)
2) D-xylose absorption test (if malabsorption then less d-xylose will be found in urine)
3) Endoscopy = villus atrophy
4) Jejunal biopsy = villus atrophy

Treat with antibiotics e.g. tropical sprue

56
Q

Which biochemical markers suggest a patient with anorexia is at risk of re-feeding syndrome?

A

Low phosphate
Low K
Low magnesium
Abnormal fluid balance

57
Q

Clinically how do we differentiate between gastric and duodenal ulcers?

A 
Gastric = worse on eating
Duodenal = worse when hungry, relieved bu eating
58
Q

Remeber hepatitis D superinfection is an important differential in a Hep B patient who suddenly deteriorates

A

Superinfection is high risk of fulminant hepatitis, chronic hepatitis and cirrhosis

59
Q

Why is a cirrhosis liver ‘bumpy’ rather than the smooth contour of a healthy liver?

A

Due to the presence of regenerative nodules which the liver utilises to try and overcome the damage

60
Q

What are the components of a portal triad?

A

Portal artery
Portal vein
Bile duct

61
Q

What is the main function of stellate cells?

A

Normally they store vitamin a

When there is injury, the hepatocytes release factors which trigger the stellate cells to form fibrinogen —> fibrosis

62
Q

Why does cirrhosis cause portal hypertension?

A

In response to damage, stellate cells produce fibrin which compresses the portal vein —> increased pressure

63
Q

Ascites = caused by portal hypertension forcing fluid into the peritoneal cavity

A

Splenomegaly = caused by cirrhosis due to fluid etc backing up as cannot get into the scarred liver

The liver is high pressure —> blood is diverted away from liver to the kidney —> too much blood —> renal failure

64
Q

Why do people with cirrhosis developed gynaecomastia, spider naevi and palmar erythema?

A

The liver plays an important role in the metabolism oestrogen into substances which can be excreted. In cirrhosis, this does not happen and oestrogen levels rise

65
Q

Features of cirrhosis

A
  • portal hypertension
  • jaundice + pruritis
  • hepatic encephalopathy
  • clotting problems -> bruising
  • ascites

Gold standard investigation is biopsy

66
Q

What is the most sensitive and specific test for the diagnosis of liver cirrhosis in patients with chronic liver disease?

A

Platelets
Thrombocytopenia

(Typically AST would be 2.5 times ALT, and urea would be low as this is produced by the liver)

67
Q

Remember copper and caeruloplasmin in Wilsin’s disease is LOW as the copper has been deposited in the tissues

A

Penicillamine is treatment of choice!

68
Q

Non-variceal bleed = do NOT give PPI prior to endoscopy as it can mask bleeding site. PPI e.g. omeprazole 80mg can be given after endoscopy to reduce risk of re-bleed

A

Varices bleed = give terlipressin and prophylactic ABx prior to endoscopy.

69
Q

How do you differentiate between type 1 and 11 autoimmune hepatitis?

A

1) ANA, anti-smooth muscle, low albumin and high PT time (also this is by far the most common type)
2) ALKM-1 (anti-liver or kidney microsome) or ALC-1 (liver cytosol) (mainly in young girls)

70
Q

When patients have a large volume of ascitic fluid removed they a re given albumin ‘cover’ e.g. an albumin infusion. Why?

A

To prevent circulatory dysfunction and mortality

71
Q

AFP is a marker for hepatocelullar cancer

A

CA19-9 is a marker for pancreatic cancer

72
Q

How do you treat H.pyloi infection?

A

PPI + amoxicillin + metronidazole (MAP)

If penicillin allergic then PPI + metronidazole + clarithromycin

73
Q

LDH is very raised in liver metastases and obstructive jaundice

A

LDH is very raised in liver metastases and obstructive jaundice

74
Q

The liver makes clotting factors I, II, V, VII, IX-XIII

A

Don’t forget it also makes albumin!

75
Q

The Child-Pugh scoring system is used for cirrhotic patients. What does it include?

A

ABCDE

Albumin
Bilirubin 
Clotting (INR)
Distension (ascites?)
Encephalopathy

A score of 5-6 = A, 7-9 = B and 10-15 = C

76
Q

Name the 3 types of acute liver failure?

A
  • Fulminant = encephalopathy develops with 1 week
  • Acute = encephalopathy develops within 2-4 weeks
  • Sub-acute = encephalopathy develops within 4-8 weeks
77
Q

Budd-Chiari syndrome is venous outflow obstruction —> increased sinusoidal pressure and portal hypertension. How does it present?

A

Classic triad of ascites, Abdo pain and hepatomegaly

Remember it is most common in hypercoagulable states e.g. myeloproliferative disorders

78
Q

What is a TIPS procedure?

A

Transjugular intrahepatic portosystemic shunt

A radiologist inserts a catheter that connects the portal and hepatic vein to bypass the dodgy liver and try to relieve some symptoms

79
Q

Hep A is an RNA virus spread faecal oral and DOES NOT cause cirrhosis

A

Hep E is and RNA virus spread via faecal oral. 20% of pregnant women will develop fulminant hepatic failure if infected

80
Q

Hep B is a DNA virus spread via sex, blood etc. Similar clinical picture to Hep A but often more severe. What does the serology mean)

A

HBsAg = 1st serological marker e.g. infectious

HBsAb = remains permanently after infection e.g. means you are immune

HBcAb = detectable 1-2 weeks after acute infection (IgM first then IgG)

81
Q

90% of patients will clear HBV —> 10% will be chronically infected. Which serological marker is +ve in chronically infected people?

A

HBsAg

Of the carriers, 10-20% of carriers develop cirrhosis and there is an increased risk of HCC

82
Q

How can you tell if a patient is immune due to past infection OR immune due to immunisation?

A

Immune people = HBsAb

If they have been previously infected then HBcAb (IgG) will also be present

83
Q

HCV is an RNA virus spread parenterally. >80% will develop a chronic infection and around 30% develop cirrhosis

A

Treatment is with an anti-viral e.g. peginterferon or ribavirin

84
Q

Piecemeal necrosis with +ve anti-smooth muscle/ anti-LKM

A

Autoimmune hepatitis

85
Q

Anti-mitochondrial antibody???

A

PBC - primary biliary cirrhosis

Causes symptoms as the bile duct cells are damaged allowing bile to leak out —> irritation and liver inflammation

E.g. jaundice, itch, xanthoma (cholesterol leaks out), joint pain (other autoimmune disease ?). High ALP and GGT

86
Q

Why does PSC cause a beaded appearance on imaging?

A

There are areas of fibrosis, interspersed with areas of dilatation of the bile ducts. This can compress the portal vein —> portal hypertension and cirrhosis

There is chronic inflammation and damage to the bile duct —> increased risk of cholangiocarcinoma

Also called ‘onion skin fibrosis’ due to layers of inflammation and fibrosis around a bile duct

80% of patients with PSC = pANCA +ve
High ALP and GGT

87
Q

In HFE, there is a high ferritin, iron and transferrin saturation

A

Remember it is autosomal recessive due to a mutation in the HFE gene

88
Q

What are the features of Wilson’s disease?

A

Related to the site of copper deposition:

  • liver = cirrhosis
  • blood = haemolysis
  • eyes = ophthalmia
  • psych = personality change/ behaviour problems
  • brain = ataxia, seizures, tremor etc
89
Q

Hydrated cysts are usually caused by a tapeworm. They can cause RUQ pain as the cyst enlarges

A

10% degree spontaneously but others will need surgical removal

If they rupture there will be an anaphylactic reaction

90
Q

Hepatic adenaoma are benign, solitary tumours often found in the right lobe of th liver in women taking the OCP. Usually incidental

A

Remember that symptoms such as weight loss, fatigue etc, mass on liver and raised AFP = hepatocellular carcinoma until proven otherwise!

91
Q

Endoscopic ligation is 1st line in oesophageal varices

A

For gastric varices, infection with N-butyl-2-cyanoacrylate is 1st line

92
Q

In haemochromatosis, transferrin and ferritin levels are high. Why is TIBC low?

A

TIBC is low because it is a measure of how many binding sites are available - if excess iron is bound then this will be low

93
Q

Wilson’s disease causes excess copper deposition in the tissue —> reduced serum caeruloplasmin and serum copper

A

There is also increased 24 hour urinary copper excretion

94
Q

How is spontaneous bacterial peritonitis diagnosed>

A

Clinical ascites
Diagnostic tap:
WCC > 250 cells/ mm3
AND >90% polymorph

If the patient is unwell treat with piperacillin/ tazobactam

If not unwell the treat with co-trimoxazole

95
Q

What is the best diagnostic investigation for suspected carcinoid syndrome?

A

Urinary 5-HIAA as carcinoid tumours release serotonin

The management of carcinoid syndrome is with somatostatin analogues such as octreotide

96
Q

What is the main risk factor for adenocarcinoma of the oesophagus?

A

Barret’s (usual squamous epithelium is replaced by columnar)

97
Q

Which drug can be used for patients in advanced liver cancer that are not suitable for surgery?

A

Sorafenib (a multikinase inhibitor)

98
Q

How do you differentiate between acute dystonia and tardive dyskinesia?

A

Acute dystonia = spastic contraction which occurs within hours to days of drug e.g. oculogyric crisis

Tardive dyskinesia = abnormal, involuntary movements of the lips, tongue, trunk etc which develops after months of continuous use e.g. lip smacking

99
Q

Ischaemic colitis presents with Abdo pain, PR bleeding and diarrhoea. It is most common in older, arteriopaths. What part of the bowel is most commonly affected?

A

Splenic flexures

This is a watershed area e.g. where one arterial blood supply changes to another (SMA to IMA)

100
Q

Drain pipe colon

A

Associated with UC

Rose thorn ulcers = associated with Crohn’s

101
Q

What advice should be given to patients BEFORE testing them for H.pylori?

A

They MUST stop:

  • PPI for 2 weeks before
  • Abx for 4 weeks before
  • H2 receptor antagonist 1 day before

The urea breath test is used to confirm H. Pylori eradication

102
Q

Don’t forget the pancreas mnemonic for severity of pancreatitis!

A 
P = PaO2 <8
A = AGE > 55
N = Neutrophils >15
C = calcium < 2
R = renal function (UREA >16)
E = enzymes (LDH)
A = Albumin 
Sugar = BM >10
103
Q

Rye contains gluteun

A

Maize is gluteun free

104
Q

Look up cyclical vomiting syndrome

A

It is associate with migraines

105
Q

Likely diagnosis in a patient with metabolic acidosis + low or normal glucose?

A

Alcoholic ketoacidosis

General Medicine (6 decks)

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