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Medicine finals Prithvi > GI + Liver > Flashcards

GI + Liver Flashcards

1
Q

common causes of raised Alkaline phosphate

A

ALKPHOS -

  • Any fracture
  • Liver damage (post-hepatic jaundice)
  • Kancer (cancer)
  • Paget’s disease of the bone; Pregnancy
  • Hyperparathyroidism
  • Surgery
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2
Q

Give 4 causes of hepatitis/cirrhosis

A
  1. Alcohol
  2. viruses (Hepatitis A-E, EBV, CMV)
  3. drugs (paracetamol overdose, rifampicin, statins)
  4. Autoimmune (Autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis)
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3
Q

Which drugs can cause cholestasis?

A

flucloxacillin, co-amoxiclav, nitrofurantoin, sulphonylureas and steroids

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4
Q

what is hereditary haemochromatosis?

A

autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation.

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5
Q

diagnostic test for hereditary haemochromatosis

A

molecular genetic testing for the C282Y and H63D mutations

liver biopsy: Perl’s stain

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6
Q

Typical iron study profile in patient with haemochromatosis

what can joint x-rays show?

A

transferrin saturation > 55% in men or > 50% in women
raised ferritin (e.g. > 500 ug/l) and iron
low TIBC

**Joint x-rays characteristically show chondrocalcinosis

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7
Q

management of hereditary haemochromatosis

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

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8
Q

symptoms to ask for in HPC for GI conditions -

A 
Abdominal pain
Difficulty swallowing
Reflux
Nausea/Vomiting
Bowel Habit alteration
Blood loss
unintentional Weight loss
Fevers
Nocturnal symptoms

….then expand appropriately

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9
Q

additional quesns to ask if someone has difficulty swallowing?

A

is it solids only or fluids or both that are difficult to swallow?
when did it start?
has it progressed?

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10
Q

additional quesns to ask if someone has nausea/vom?

A

how often?

contents - blood, bile, food, etc.

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11
Q

additional quesns to ask if someone has altered bowel habits?

A

what is normal for them - frequency and consistency and how is it now?
any blood? - if yes then is it fresh or mixed into the poo

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12
Q

what do nocturnal symptoms signify?

A

if someone is waking up in the night to open their bowels or with pain, then this worrying and points more towards an organic bowel condition like IBD or cancer

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13
Q

if you suspect or pt has liver disease, what questions are important to ask in PMH and social hx?

A

previous blood transfusions, tattoos, foriegn travel

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14
Q

what test is important to do in someone with chronic lower GI symptoms?

A

stool faecal calprotectin

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15
Q

what stool test is important to do in someone with upper GI dyspeptic symptoms?

A

stool H.pylori antigen test

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16
Q

how many stool cultures do u need to do?

A

3

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17
Q

how to interpret faecal calprotectin results?

A

<50 - normal. high NPV so unlikely IBD
>150 - refer to gastro
intermediate - repeat in 1 month and refer if it remains elevated

18
Q

what are some alarm features with regards to GI disease that will require further investigations for organic diseases

A

hx -dysphagia, blood loss, weight loss, nocturnal symptoms, age>45, family history of IBD, GI cancer, acutely unwell, recent onset of symptoms

exam -
Jaundice
Abnormal mass
Lymphadenopathy

tests -
Deranged bloods e.g. Anemia, LFTs, CRP
Positive coeliac serology
Raised faecal calprotectin

19
Q

ddx for dysphagia?

A

structural - oesophageal cancer, benign stricture, reflux oesophagitis

motility - achalasia, aperistalsis, oesophageal spasm

19
Q

ddx for dysphagia?

A

structural - oesophageal cancer, benign stricture, reflux oesophagitis

motility - achalasia, aperistalsis, oesophageal spasm

20
Q

what are peptic ulcers?

A

Peptic ulcers involve ulceration of the mucosa of the stomach (gastric ulcer) or the duodenum (duodenal ulcer). Duodenal ulcers are more common.

21
Q

what is the protective layer in the stomach comprised of and what can it be broken down by?

A

There is a protective layer in the stomach comprised of mucus and bicarbonate secreted by the stomach mucosa. This protective layer can be broken down by:

Medications (e.g. steroids or NSAIDs)
Helicobacter pylori
22
Q

increased acid in the stomach or consequently the duodenum can result from?

A 
Stress
    Alcohol
    Caffeine
    Smoking
    Spicy foods
23
Q

presentation of peptic ulcer disease

A

Epigastric discomfort or pain
Nausea and vomiting
Dyspepsia
Bleeding causing haematemesis, “coffee ground” vomiting and melaena
Iron deficiency anaemia (due to constant bleeding)

24
Q

how to differentiate gastric ulcer from duodenal?

A

In your MCQ exams, eating typically worsens the pain of gastric ulcers and improves the pain of duodenal ulcers.

25
Q

what type of epithelial lining does the oesophagus have and what type of lining does the stomach have?

A

The oesophagus has a squamous epithelial lining . The stomach has a columnar epithelial lining

26
Q

presentation of GORD

A

Dyspepsia is a non-specific term used to describe indigestion. It covers the symptoms of GORD:

    Heartburn
    Acid regurgitation
    Retrosternal or epigastric pain
    Bloating
    Nocturnal cough
    Hoarse voice
27
Q

management of GORD

A 
lifestyle advice - 
    Reduce tea, coffee and alcohol
    Weight loss
    Avoid smoking
    Smaller, lighter meals
    Avoid heavy meals before bed time
    Stay upright after meals rather than lying flat

antacids when required
PPIs
H2RAs

surgery - laparoscopic fundoplication

28
Q

what is barretts oesophagus

A

metaplasia of lower oesophageal epithelium from squamous to columnar epithelium as a result of constant reflux of acid.
Barretts oesophagus is considered a “premalignant” condition and is a risk factor for the development of adenocarcinoma of the oesophagus.
**when this happens, patients typically get an improvement in reflux symptoms

29
Q

how are ppl with barretts oesophagus monitored?

A

regular endoscopy to monitor for adenocarcinoma. In some patients there is a progression from Barretts oesophagus (columnar epithelium) with no dysplasia to low grade dysplasia to high grade dysplasia and then to adenocarcinoma.

30
Q

tx of barretts oesophagus

A

PPIs

Ablation treatment during endoscopy using photodynamic therapy, laser therapy or cryotherapy is used to destroy the epithelium so that it is replaced with normal cells. This is not recommended in patients with no dysplasia but has a role in low and high grade dysplasia in preventing progression to cancer.

31
Q

h pylori

A

gram -ve bacteria. damages gastric mucosa causing gastritis and increases risk of ulcers and stomach cancer. it also produces ammonia to neutralise the stomach acid which also damages the epithelial cells.

Anyone with dyspepsia is offered a H.pylori test and this needs 2 weeks without using PPI before testing for h.pylori

32
Q

what test is used to diagnose h.pylori

A

H.pylori stool antigen test

urea breath test can also be used
rapid urease test can be performed during endoscopy.

33
Q

how is h.pylori treated?

A

triple-therapy regimen that comprises a proton pump inhibitor and 2 antibacterials.

in general -
1. pts with no penicillin allergy - A proton pump inhibitor, plus amoxicillin, and either clarithromycin or metronidazole (treatment choice should take into account previous treatment with clarithromycin or metronidazole) for 7 days

  1. penicillin allergy - A proton pump inhibitor, plus clarithromycin, and metronidazole fir 7 days
34
Q

management of peptic ulcers

A

diagnosed using upper GI endoscopy. During endoscopy a rapid urease test (CLO test) can be performed to check for H. pylori. Biopsy should be considered during endoscopy to exclude malignancy as cancers can look similar to ulcers during the procedure.

Medical treatment is the same as with GORD, usually with high dose proton pump inhibitors. Endoscopy can be used to monitoring the ulcer to ensure it heals and to assess for further ulcers.

35
Q

complications of PUD

A

Bleeding from the ulcer is a common and potentially life threatening complication.

Perforation resulting in an “acute abdomen” and peritonitis. This requires urgent surgical repair (usually laparoscopic).

Scarring and strictures of the muscle and mucosa. This can lead to a narrowing of the pylorus (the exit of the stomach) causing difficulty in emptying the stomach contents. This is known as pyloric stenosis. This presents with upper abdominal pain, distention, nausea and vomiting, particularly after eating.

36
Q

what medications put u at risk of duodenal ulcers?

A

nsaids
steroids
SSRIs

37
Q

in ppl presenting with dyspepsia, who require urgent endoscopy?

A

everyone with dysphagia
those >/=55 with ALARM Symptoms or persistent/refractory symptoms

ALARM Symptoms - 
Anaemia
Loss of weight
Anorexia
Recent onset/progressive symptoms
Melaena/haematemesis
Swallowing difficulties
38
Q

functional dyspepsia management (INCOMPLEYTE)

A

it is common
eradicate H.pylori if present
PPIs, psychotherapy and low dose amitryptyline may help

39
Q

complications of GORD

A 
oesophagitis
benign strictures
ulcers
iron deficiency
barretts oesophagus
40
Q

causes of GORD

A 
lower oesophageal sphincter hypotension
hiatus hernia (common in pts >50 esp obese pts)
obesity
oesophageal dysmotility
gastric acid hypersecretion
smoking
alcohol
pregnancy

Medicine finals Prithvi (22 decks)

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