GI Medicine 4 Flashcards
Melanosis coli
- What is it?
- What can cause it?
- pigmentation of the bowel wall
2. laxatives especially anthraquinone compounds (e.g. senna)
Metabolic alkalosis
What can cause it?
Na+ causes:
- vomiting / aspiration
- diuretics
- increased adrenal action: cushing’s or primary hyperaldosteronism
- liquorice / carbenoxolone
K+ causes:
- hypokalaemia
- Bartter’s syndrome
NOTE:
pathophysiology:
Na+: low sodium causes activation of RAA system to reabsorb Na+ in kidney - H+ is exchanged for the reabsorption of Na+
K+: low K+ causes movement of K+ out of cells to keep ECF concentration. Again, this is done in exchange for H+ to maintain neutrality
Metoclopramide
- What can it be used for?
- What are its side effects?
- When should be avoided?
- anti-emetic
- GORD
- pro kinetic action means can be used for gastroparesis in diabetic neuropathy
- pro kinetic action can help analgesic absorption in migraine too
- extrapyramidal SEs
- hyperprolactinaemia
NOTE: this is because has very similar target and mechanism of action to antipsychotics
- bowel obstruction
Molecular biology
What is detected by the following techniques?
- a) southern blotting
b) northern blotting
c) western blotting - ELISA (enzyme-linked immunosorbent assay)
- a) DNA
b) RNA
c) proteins
SNOW
DROP
- antigens or antibodies
(colour changing enzyme is attached to:
- antigen if looking for antibody
- antibody if looking for antigen)
Non-Alcoholic Fatty Liver Disease
- What pathophysiology processes can it include?
- What can it be associated with?
- What clinical features are seen on
a) exam
b) bloods
c) US - What investigation is done?
- What is the management?
- steatosis - fat in the liver
- steatohepatitis - fat + inflammation in the liver
- progressive disease may cause fibrosis + liver cirrhosis
- obesity
- hyperlipidaemia
- type 2 diabetes
- jejunoileal bypass
- sudden weight loss / starvation
- a) hepatomegaly
b) ALT>AST
c) echogenic liver - ELF (enhanced liver fibrosis) blood test
-> measures combination of hyaluronic acid, procollagen III, tissue inhibitor of metalloproteinase 1 - lifestyle - most important is to lose weight
Oesophageal Cancer
- Where is each type most likely to occur:
a) adenocarcinoma
b) squamous cell carcinoma - What are the RFs for?
a) adenocarcinoma
b) squamous cell carcinoma
c) both - What clinical features are seen?
- a) at gastro-oesophageal junction
b) upper 2/3rds - a)
- GORD
- barrett’s
- obesity
b)
- alcohol
- nitrosamines (fish) in diet
- Plummer-Vinson syndrome (triad of dysphagia secondary to oesophageal webs, iron-deficiency anaemia + glossitis)
c)
- smoking
- achalasia
THINK: adenocarcinoma is going to be at the gastro-oesophageal junction and GORD/barrett’s be RFs because reflux = GORD = change FROM the squamous cells to columnar epithelium so osly therefore would not be a squamous cell cancer)
3.
- dysphagia
- vomiting
- anorexia + weight loss
Pancreatic Cancer
- What type and where is the typical tumour?
- What clinical features are seen?
- What is the gold-standard investigation?
- adenocarcinoma at the head of the pancreas
- painless jaundice
- cholestatic picture: raised ALP, pale stools, dark urine
- general symptoms: anorexia, weight loss, epigastric or atypical back pain
loss of exocrine function: e.g. steatorrhea
loss of endocrine function: e.g. diabetes
- CT scan
- may see ‘double duct’ sign caused by enlargement of common bile and pancreatic ducts
Peptic Ulcer Disease
1.
a) What are the majority of peptic ulcers associated with?
b) What else can they be associated with?
- What clinical features are seen in
a) both
b) gastric
c) duodenal - What investigation is done?
- How is it managed?
- a) h. pylori
b)
- NSAIDs
- SSRIs
- corticosteroids
- bisphosphonates
2.
a) epigastric pain + nausea
b) pain worsened by eating
c) pain worse when hungry, relieved by eating
- test for h.pylori - urea breath test or stool antigen
- PPI
+ if h. pylori positive then add amoxicillin and one of clarithromycin OR metronidazole
Peptic Ulcer Perforation
- What clinical feature is seen?
- What investigation can be done?
- sudden onset abdominal pain becoming more generalised
2. erect AXR - 75% of will have air under the diaphragm
Peptic Ulcer Acute bleeding
- What is this often due to?
- How is it managed?
- erosion into the gastroduodenal artery
- ABCDE
- IV protein pump inhibitor
- organise endoscopic intervention
Primary Biliary Cholangitis
- What is it associated with?
- What clinical features are seen?
- How is diagnosis made?
- How is it managed?
- What complications can be seen?
- sjogren’s (up to 80%)
- Rheumatoid arthritis
- systemic sclerosis
- thyroid disease
2. early: - asymptomatic with cholestatic LFTs - fatigue - pruritus \+/- jaundice \+/- RUQ pain
late:
- cirrhosis
- hepatosplenomagely
- clubbing
- immunology:
- IgM
- anti-mitochondrial antibodies (AMA) - highly sensitive + specific
- smooth muscle antibodies in 30%
imaging: US or MRCP
- ursodeoxycholic acid (slows disease + improves symptoms)
- if pruritus: cholestyramine
- fat soluble vitamin supplementation
THINK: CHOLic acid due to CHOLestasis
- cirrhosis - liver failure - ascites/oesophageal varices
- increased risk (x20) of hepatocellular carcinoma
- osteomalacia + osteoporosis
mnemonic: the M rule - IgM - anti-mitochondrial antibodies - Middle aged females
Primary sclerosing Cholangitis
- What happens in the disease?
- What clinical features can be seen?
- What investigations can be done?
- What are the possible complications?
- What is it associated with
- inflammation and fibrosis of extra-hepatic bile ducts
- cholestatic LFTs
- fatigue
- pruritus
- jaundice
- RUQ pain
- MRCP: biliary strictures giving biliary tree “beaded” appearance
(ERCP if MRCP contraindicated) - p-ANCA may be positive
- liver biopsy has onion skin appearance
- MRCP: biliary strictures giving biliary tree “beaded” appearance
- increased risk of cholangiocarcinoma (10%!) and colorectal cancer
- UC (80% with PSC have UC)
- Crohn’s
- HIV
Pernicious Anaemia
- What is it?
- What are RFs?
- What clinical features can be seen?
- What is seen on investigation?
- How is it treated?
- What are they at increased risk of?
- antibodies to intrinsic factor +/- parietal cells leads to decreased B12 absorption
NOTE: B12 important for RBC formation and myelination of nerves
- autoimmune disease
- group A blood type
- anaemia: lethargy, pallor, breathlessness
neurological features:
- peripheral neuropathy
- subacute combined degeneration of the spinal cord: parathesiae, ataxia, progressive weakness
- psychiatric features (e.g. irritability, confusion, depression)
other:
- lemon-yellow tinge to skin
- glossitis
- blood: macrocytic anaemia + low B12
blood film: hyperhsegmented polymorphs
anti-intrinsic factor antibody (only seen in 50% but highly specific)
NOTE: gastric parietal cell antibody in some patients but not specific: think definition of disease is intrinsic factor antibodies +/- gastric parietal cell therefore they will not be the main antibody if +/-
- vit B12 +/- folate IM injections (give more if neuro features)
- gastric cancer
Peutz-Jehgers Syndrome
- What is it?
- What clinical features can be seen?
- autosomal dominant condition with hamartuous polyps in GI tract (mostly small bowel) and pigmented freckles on lips, face, palms + soles
- intestinal obstruction
- GI bleeding
- GI cancer (but polyps themselves are not pre-malignant)
