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
Management of a mild attack of Crohns’
Oral prednisolone | 30mg/d PO for 1 week then 20mg/d for 4 weeks then reduce by 5mg gradually if symptoms resolved
26
Management of severe Crohns flare
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
27
What is the role of azathioprine in Crohn’s disease?
Largely for steroid sparing Also used for triple therapy which is very effective - steroids + infliximab + azathioprine
28
Indications for surgery in Crohns
1) Stricture causing obstruction 2) Perforation 3) Medication failure 4) Fistulae 5) Abscesses
29
Give 5 causes of liver failure
1) Infection - hepatitis 2) Alcohol 3) Toxins - paracetemol 4) Vascualr - trauma/ bud Chiarri 5) Autoimmune 6) Other syndromes e.g. haemochromatosis etc
30
In patients with liver failure, hypoglycaemia is a big risk
Give 10% glucose IV 1L/2h and measure BM regularly
31
Remember that warfarin effects are increased by liver failure
Avoid hepatotoxic drugs such as paracetemol and methotrexate when prescribing in liver failure
32
What causes hepatic encephalopathy?
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
33
Indications for transplant after paracetemol induced liver failure?
Arterial pH <7.3, 24 hours after ingestion OR Raised prothrombin time (PT) Creatinine >300 Grade 3/4 encephalopathy
34
List 5 causes of liver cirrhosis
``` Chronic alcohol abuse Chronic HBV/ HCV Haemochromatosis Autoimmune disease e.g. primary sclerosing cholangitis Hepatic vein event e.g. Budd chairing ```
35
Leuconycia
White nails due to hypoalbuminaemia (usually chronic liver disease)
36
Advice for alcohol consumption
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
37
List 4 acute effects of alcohol excess
1) CNS impairment —> alcohol and violence 2) Oesophagitis 3) Acute oesophagitis 4) Respiratory depression/ aspiration
38
Discuss the progression of alcoholic liver disease
Fatty changes —> fibrosis —> cirrhosis —> hepatocellular carcinoma
39
List some signs of chronic liver disease
``` Spider naevi Encephalopathy Hypoalbuminaemia Prolonged PT Portal hypertension ```
40
What is the portal hypertension? What are the signs?
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
41
The Child’s Pugh score is used to classify cirrhosis. What are the components?
1) Ascites 2) Encephalopathy 3) Albumin level 4) Prothrombin time 5) Bilirubin level A score of 10-15 is decompensated cirrhosis
42
Ascites results from peripheral arterial vasodilatation and portal hypertension. Na and water retention as well as hypoalbuminaemia is also important. List 4 causes:
Liver cirrhosis Malignancy e.g. GI tract/ ovarian Heart failure Nephrotic syndrome
43
What is the commonest liver disease?
NAFLD | Treatment is diet and exercise but this rarely happens
44
Most likely diagnosis in a 40 year old lay presenting with fatigue, itch without rash and xanthelasma. How do you confirm?
PBC Primary biliary cholangitis AMA- anti-mitochondrial antibodies Cholestatic LFT - alk phos and GGT are very raised Liver biopsy
45
What is the treatment for PBC?
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
Piecemeal necrosis and lobular involvement on liver biopsy with interface hepatitis
Autoimmune hepatitis
47
Which autoantibodies are associated with type 1 auto-immune hepatitis?
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
Which autoantibodies are associated with type 2 autoimmune hepatitis?
Anti-liver kidney microsomal 1 (LKM-1) Remember typically presents as per viral hepatitis
49
What is the treatment of autoimmune hepatitis?
Corticosteroids + azathioprine Serious condition - 40% will develop cirrhosis and 50% will develop oesophageal varices in 2 years
50
40% of patients with primary sclerosing cholangitis have UC
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
What is the differential for malabsorption?
- Coeliac - CF - Crohn’s - Short bowel - tropical sprue - chronic pancreatitis
52
What is a SeHCAT scan?
A radionucloetide scan which tests for bile acid malabsorption
53
Features of Whipple’s disease?
- 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
H. Pylori is associated with 90% duodenal ulcers GI bleed, perforation and gastric outlet obstruction are all complications of peptic ulcer disease
H.pylori associated with 75% gastric ulcers
55
Other than blood tests such as FBC, which other tests are used in the diagnosis of tropical sprue?
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
Which biochemical markers suggest a patient with anorexia is at risk of re-feeding syndrome?
Low phosphate Low K Low magnesium Abnormal fluid balance
57
Clinically how do we differentiate between gastric and duodenal ulcers?
``` Gastric = worse on eating Duodenal = worse when hungry, relieved bu eating ```
58
Remeber hepatitis D superinfection is an important differential in a Hep B patient who suddenly deteriorates
Superinfection is high risk of fulminant hepatitis, chronic hepatitis and cirrhosis
59
Why is a cirrhosis liver ‘bumpy’ rather than the smooth contour of a healthy liver?
Due to the presence of regenerative nodules which the liver utilises to try and overcome the damage
60
What are the components of a portal triad?
Portal artery Portal vein Bile duct
61
What is the main function of stellate cells?
Normally they store vitamin a When there is injury, the hepatocytes release factors which trigger the stellate cells to form fibrinogen —> fibrosis
62
Why does cirrhosis cause portal hypertension?
In response to damage, stellate cells produce fibrin which compresses the portal vein —> increased pressure
63
Ascites = caused by portal hypertension forcing fluid into the peritoneal cavity
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
Why do people with cirrhosis developed gynaecomastia, spider naevi and palmar erythema?
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
Features of cirrhosis
- portal hypertension - jaundice + pruritis - hepatic encephalopathy - clotting problems -> bruising - ascites Gold standard investigation is biopsy
66
What is the most sensitive and specific test for the diagnosis of liver cirrhosis in patients with chronic liver disease?
Platelets Thrombocytopenia (Typically AST would be 2.5 times ALT, and urea would be low as this is produced by the liver)
67
Remember copper and caeruloplasmin in Wilsin’s disease is LOW as the copper has been deposited in the tissues
Penicillamine is treatment of choice!
68
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
Varices bleed = give terlipressin and prophylactic ABx prior to endoscopy.
69
How do you differentiate between type 1 and 11 autoimmune hepatitis?
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
When patients have a large volume of ascitic fluid removed they a re given albumin ‘cover’ e.g. an albumin infusion. Why?
To prevent circulatory dysfunction and mortality
71
AFP is a marker for hepatocelullar cancer
CA19-9 is a marker for pancreatic cancer
72
How do you treat H.pyloi infection?
PPI + amoxicillin + metronidazole (MAP) If penicillin allergic then PPI + metronidazole + clarithromycin
73
LDH is very raised in liver metastases and obstructive jaundice
LDH is very raised in liver metastases and obstructive jaundice
74
The liver makes clotting factors I, II, V, VII, IX-XIII
Don’t forget it also makes albumin!
75
The Child-Pugh scoring system is used for cirrhotic patients. What does it include?
ABCDE ``` Albumin Bilirubin Clotting (INR) Distension (ascites?) Encephalopathy ``` A score of 5-6 = A, 7-9 = B and 10-15 = C
76
Name the 3 types of acute liver failure?
- Fulminant = encephalopathy develops with 1 week - Acute = encephalopathy develops within 2-4 weeks - Sub-acute = encephalopathy develops within 4-8 weeks
77
Budd-Chiari syndrome is venous outflow obstruction —> increased sinusoidal pressure and portal hypertension. How does it present?
Classic triad of ascites, Abdo pain and hepatomegaly Remember it is most common in hypercoagulable states e.g. myeloproliferative disorders
78
What is a TIPS procedure?
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
Hep A is an RNA virus spread faecal oral and DOES NOT cause cirrhosis
Hep E is and RNA virus spread via faecal oral. 20% of pregnant women will develop fulminant hepatic failure if infected
80
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)
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
90% of patients will clear HBV —> 10% will be chronically infected. Which serological marker is +ve in chronically infected people?
HBsAg Of the carriers, 10-20% of carriers develop cirrhosis and there is an increased risk of HCC
82
How can you tell if a patient is immune due to past infection OR immune due to immunisation?
Immune people = HBsAb If they have been previously infected then HBcAb (IgG) will also be present
83
HCV is an RNA virus spread parenterally. >80% will develop a chronic infection and around 30% develop cirrhosis
Treatment is with an anti-viral e.g. peginterferon or ribavirin
84
Piecemeal necrosis with +ve anti-smooth muscle/ anti-LKM
Autoimmune hepatitis
85
Anti-mitochondrial antibody???
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
Why does PSC cause a beaded appearance on imaging?
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
In HFE, there is a high ferritin, iron and transferrin saturation
Remember it is autosomal recessive due to a mutation in the HFE gene
88
What are the features of Wilson’s disease?
Related to the site of copper deposition: - liver = cirrhosis - blood = haemolysis - eyes = ophthalmia - psych = personality change/ behaviour problems - brain = ataxia, seizures, tremor etc
89
Hydrated cysts are usually caused by a tapeworm. They can cause RUQ pain as the cyst enlarges
10% degree spontaneously but others will need surgical removal If they rupture there will be an anaphylactic reaction
90
Hepatic adenaoma are benign, solitary tumours often found in the right lobe of th liver in women taking the OCP. Usually incidental
Remember that symptoms such as weight loss, fatigue etc, mass on liver and raised AFP = hepatocellular carcinoma until proven otherwise!
91
Endoscopic ligation is 1st line in oesophageal varices
For gastric varices, infection with N-butyl-2-cyanoacrylate is 1st line
92
In haemochromatosis, transferrin and ferritin levels are high. Why is TIBC low?
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
Wilson’s disease causes excess copper deposition in the tissue —> reduced serum caeruloplasmin and serum copper
There is also increased 24 hour urinary copper excretion
94
How is spontaneous bacterial peritonitis diagnosed>
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
What is the best diagnostic investigation for suspected carcinoid syndrome?
Urinary 5-HIAA as carcinoid tumours release serotonin The management of carcinoid syndrome is with somatostatin analogues such as octreotide
96
What is the main risk factor for adenocarcinoma of the oesophagus?
Barret’s (usual squamous epithelium is replaced by columnar)
97
Which drug can be used for patients in advanced liver cancer that are not suitable for surgery?
Sorafenib (a multikinase inhibitor)
98
How do you differentiate between acute dystonia and tardive dyskinesia?
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
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?
Splenic flexures This is a watershed area e.g. where one arterial blood supply changes to another (SMA to IMA)
100
Drain pipe colon
Associated with UC Rose thorn ulcers = associated with Crohn’s
101
What advice should be given to patients BEFORE testing them for H.pylori?
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
Don’t forget the pancreas mnemonic for severity of pancreatitis!
``` 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
Rye contains gluteun
Maize is gluteun free
104
Look up cyclical vomiting syndrome
It is associate with migraines
105
Likely diagnosis in a patient with metabolic acidosis + low or normal glucose?
Alcoholic ketoacidosis