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general gastro - passmed Flashcards

1
Q

what would the triad of :

  1. abdo pain
  2. ascites
  3. tender hepatomegaly

make you suspect..?
what is it?
and how would you investigate it?

A

budd-chiari syndrome
thrombosis of hepatic vein
USS with doppler flow studies of hepatic vein

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2
Q

Budd chiari syndrome causes:

A

anything pro-coagulant…

PRV / thrombophilia / pregancy / COCP

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3
Q
  1. raised bili, ALP and ALT + abdo pain + ascites + tender hepatomegaly
A
  1. budd-chiari syndrome
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4
Q

liver pain, fevers, haematemesis (oesophageal /gastric varices)

A

Portal vein thrombosis - usually 2y to varices..

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5
Q
  1. raised ALT, raised AST (ALT raised more than AST usually), +/- raised bili
A

hepatitis

usually general malaise, non specific other symptoms etc…

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6
Q
  1. raised ALP (much more than others), raised GGT, raised bili
A

gallstones

both ALP and GGT are in the walls of the biliary system - released with damage..

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7
Q
  1. isolated raised bili
A

gilbert’s syndrome?

/ haemolytic disease eg. hereditary spherocytosis

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8
Q

where are

  1. alt
  2. ast
  3. alp
  4. bilirubin
  5. ggt

found and where are they

A

alt and ast are released in hepatocellular damage - ast by mitochondria - alt by cytosol

alp and ggt are increased in obstruction (usually biliary..)

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9
Q

isolated raised ALP , bony pain

A

? pagets
? sarcoma / bony mets
? ckd mbd - renal mineral bone disease

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10
Q

isolated raised ALT

A

barn door NAFLD

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11
Q

AST>ALT

may also see rise in GGT

A

Acute alcoholic hepatitis – AST>ALT (usually AST 3: ALT 1)

Sauce – AST

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12
Q

primary sclerosing cholangitis

A

https://www.youtube.com/watch?v=ZXs6FkjnBIs

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13
Q

give some common differentials of dysphagia?

and what are your key investigations?

A
  • oesophageal Ca - + wt loss, anorexia / vimiting during eating. progressive symptoms (solids to fluids)
  • oesophagitis - odynophagia but no weight loss and systemically well
  • oesophageal candidiasis -will be HIV+ve / steroid inhaler use..
  • achalasia - LOS fails to open during swallowing - dysphagia of both solids and fluids from the start - regurgitation of food - cough / aspiration pneumonia etc.
  • pharyngeal pouch - midline lump in the neck that gurgles on palpation - symptoms are dysphagia, regurgitation, aspiration and chronic cough.
  • systemic sclerosis - other features of CREST syndrome
  • mysathenia gravis - fatigueable / extraocular muscle weakness / ptosis
upper GI endoscopy
barium swallow (for motility disorders)
FBC
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14
Q

are you more likely to see Gastric parietal cell antibodies in pernicious anaemia OR Intrinsic factor antibodies

A

gastric parietal cell autoantibodies

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15
Q

hepatorenal syndrome: what is it, and how do you treat it?

A

Complication of end-stage liver disease

vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance. This results in ‘underfilling’ of the kidneys. This is sensed by the juxtaglomerular apparatus which then activates the renin-angiotensin-aldosterone system, causing renal vasoconstriction which is not enough to counterbalance the effects of the splanchnic vasodilation.

Management options:
1. CONSTRICT THE SPLANCHNIC VEINS - vasopressin analogues, for example Terlipressin, have a growing evidence base supporting their use. They work by causing vasoconstriction of the splanchnic circulation
volume expansion
2. VOLUME EXPAND - 20% albumin
3. transjugular intrahepatic portosystemic shunt
4. liver transplant..

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16
Q

what antibodies might you see raised in coeliac disease?

A

anti-tissue transglutaminase (anti-TTG)
anti-endomysial Ab
(don’t do anti-gliadin anymore…)

17
Q

which condition would you see AMA (antimitochondrial antibodies) in?

A

PBC

18
Q

what is Wilson’s disease
how does it present
what are the investigations
what is the first line treatment for it?

what are some potential compications?

A
  1. autosomal recessive
  2. XS deposition of Cu in tissues - causes Liver and Neuro problems

presents with features resulting from excessive copper deposition in the tissues, especially the brain, liver and cornea:
liver: hepatitis, cirrhosis (children tend to start with liver disease)
neurological: basal ganglia degeneration, speech, behavioural and psychiatric problems are often the first manifestations. Also: asterixis, chorea, dementia, parkinsonism (adults tend to present with neruo disease)
Kayser-Fleischer rings
renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails

Ix: 24hr Cu excretion high / nonspecifically deranged LFTs / serum copper decreased / serum caeruplasmin low (very low - pathognomic - think impaired excretion, because of low amounts of the protein that carries copper round in blood

Tx:
penicillamine (chelates copper) has been the traditional first-line treatment - chelates it - allows it to be excreted..
trientine

Fanconi’s syndrome - renal tubular acidosis caused by XS deposition of heavy metal (copper obvs..)

19
Q

how should you manage oesophageal varices?

  1. acute variceal haemorrhage
  2. prophylaxis of acute haemorrhage
A
  1. ABCD
    MAKE SURE THEY’RE CLOTTING - FFP / vitamin K
    STIMULATE HAEMOSTASIS - Terlipressin - vasoactive agent to stimulate initial haemostasis
    ABX: - eg. ciprofloxacin / levofloxacin
    LIGATE THE VARICES - endoscopic variceal band ligation
    IF STILL UNCONTROLLED BLEEDING - Sengstaken-Blakemore tube
    Transjugular Intrahepatic Portosystemic Shunt (TIPSS) if above measures fail
  2. prophylaxis of variceal haemorrhage
    - propranolol (reduces rebleeding / mortality)
    - PPI + Endoscopic variceal band ligation - 2wkly (PPI prevents
20
Q

what are the severities of UC exacerbations?

A

mild:
Fewer than four stools daily, with or without blood
No systemic disturbance
Normal erythrocyte sedimentation rate and C-reactive protein values

moderate:
Four to six stools a day, with minimal systemic disturbance

severe:
More than six stools a day, containing blood
Evidence of systemic disturbance, e.g.
fever
tachycardia
abdominal tenderness, distension or reduced bowel sounds
anaemia
hypoalbuminaemia
ADMIT TO HOSPITAL
21
Q

what are the risks of ERCP?

A

Bleeding 0.9% (rises to 1.5% if sphincterotomy performed)
Duodenal perforation 0.4%
Cholangitis 1.1%
Pancreatitis 1.5%

22
Q

what is gallstone ileus?

A

small bowel obstruction secondary to an impacted gallstone

23
Q

what does the serum albumin ascites gradient represent?

A

SAAG - if high - non peritoneal cause of ascites eg. budd-chiari / hepatic stuff. if low - intra peritoneal eg. ovarian Ca?

24
Q

what is the treatment of ascirtes?

A

Management
reducing dietary sodium
fluid restriction is sometimes recommended if the sodium is < 125 mmol/L
aldosterone antagonists: e.g. spironolactone
drainage if tense ascites (therapeutic abdominal paracentesis)
large-volume paracentesis for the treatment of ascites requires albumin ‘cover’. Evidence suggests this reduces paracentesis-induced circulatory dysfunction and mortality
paracentesis induced circulatory dysfunction can occur due to large volume paracentesis (> 5 litres). It is associated with a high rate of ascites recurrence, development of hepatorenal syndrome, dilutional hyponatraemia, and high mortality rate
prophylactic antibiotics to reduce the risk of spontaneous bacterial peritonitis. NICE recommend: ‘Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less, until the ascites has resolved’
a transjugular intrahepatic portosystemic shunt (TIPS) may be considered in some patients

25
Q

what is the management of hepatic encephalopathy?

A

Management
treat any underlying precipitating cause
NICE recommend lactulose first-line, with the addition of rifaximin for the secondary prophylaxis of hepatic encephalopathy
lactulose is thought to work by promoting the excretion of ammonia and increasing the metabolism of ammonia by gut bacteria
antibiotics such as rifaximin are thought to modulate the gut flora resulting in decreased ammonia production
other options include embolisation of portosystemic shunts and liver transplantation in selected patients

26
Q

what is Melanosis coli most commonly caused by?

A

Melanosis coli is most commonly caused by prolonged laxative use

27
Q

what is the treatment of pernicious anaemia?

A

3 monthly treatment of vitamin B12 injections. Folic acid supplementation may also be required.

28
Q

peptic ulcer disease.
1. what is the most common and serious location of a bleed (and also the duodenal blood supply…)

  1. how would you manage acute haematemesis due to a peptic ulcer
A
  1. gastroduodenal artery
  2. ABC approach as with any upper gastrointestinal haemorrhage
    IV proton pump inhibitor
    the first-line treatment is endoscopic intervention
    if this fails (approximately 10% of patients) then either:
    urgent interventional angiography with transarterial embolization or
    surgery
29
Q

how would you investigate a patient with incidental finding of NAFLD? (eg isolated raised ALT)

A

In patients with non-alcoholic fatty liver disease, enhanced liver fibrosis (ELF) testing is recommended to aid diagnosis of liver fibrosis - looking for more serious disease

30
Q

differentiating between an upper and a lower GI bleed

A

A bleed which occurs in the oesophagus, stomach or duodenum is classed as an upper GI bleed. Causes of upper GI bleeds include peptic ulcer or oesophageal varices. In upper GI bleeding, an increased urea level occurs due to the breakdown of red blood cells in the stomach. Melaena is usually indicative of an upper GI bleed but can occur with lower GI bleeding, though this is rare. Haematochezia is the passage of fresh blood from the rectum and usually occurs with lower GI bleeding though can occur with large upper GI bleeds. Abdominal pain is a feature of both upper and lower GI bleeding

31
Q

which patients need ABx to prevent surgical site infections?

A

clean surgery involving the placement of a prosthesis or implant
clean-contaminated surgery
contaminated surgery
surgery on a dirty or infected wound (requires antibiotic treatment in addition to prophylaxis)

32
Q

which antibiotics are linked to c dif?

what are the features of c diff?

what is the diagnostic test?

what is the management

A 
Features
diarrhoea
abdominal pain
a raised white blood cell count is characteristic
if severe toxic megacolon may develop

test: detecting Clostridium difficile toxin (CDT) in the stool (NB - antigen is not a reliable test - anyone who’s ever been exposed can have that….)

Mx: oral metronidazole 10 days -14 days
may need vancomicin if don’t respond
for life-threatening infections a combination of oral vancomycin and intravenous metronidazole should be used

33
Q

how would you diagnose liver cirrhosis?

A

Fibroscan - transient elastography

for patients with NAFLD, NICE recommend using the enhanced liver fibrosis score to screen for patients who need further testing

34
Q

what tests should you do in someone diagnosed with liver cirrhosis?

A

Further investigations
NICE recommend doing an upper endoscopy to check for varices in patient’s with a new diagnosis of cirrhosis
liver ultrasound every 6 months (+/- alpha-feto protein) to check for hepatocellular cancer

35
Q

a patient presenting with the classic triad of: jaundice and pruritus right upper quadrant pain and fatigue

a. what do you suspect
b. what might it be associated with?
c. what investigations can you do to confirm the Dx
d. what is the main complication?

A

a. primary sclerosing cholangitis

b. 80% of people with PSC have UC
sometimes PSC presents before the UC presents

c. endoscopic retrograde cholangiopancreatography (ERCP) or magnetic resonance cholangiopancreatography (MRCP) are the standard diagnostic investigations, showing multiple biliary strictures giving a ‘beaded’ appearance

d.cholangiocarcinoma in 10%
increased risk of colorectal Ca

36
Q

which vitamin is teratogenic in high doses?

A

vit A

37
Q

what are the following AXR signs classical of:

  1. coffee-bean sign
  2. multiple dilated loops of small bowel AND air in the biliary tree.
A
  1. sigmoid volvulus
  2. gallstone ileus (gallstone blocks the small bowel by lodging in ileocaecal valve - usually on a background of chronic cholecystitis
38
Q

tumour markers - which markers are for which cancer?

  1. A-FP
  2. carcinoembryonic antigen
  3. CA19-9
A
  1. Raised AFP can be a useful diagnostic marker for HCC
  2. CEA is used mostly as a marker for bowel cancer
  3. CA 19 - 9 is used mostly as a marker for pancreatic cancer.

GI (4 decks)

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