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MCCQE1 > Medicine- gastroenterology > Flashcards

Medicine- gastroenterology Flashcards

1
Q

The three stages of alcoholic liver disease

A
  1. Alcohol related fatty liver Drinking leads to a build-up of fat in the liver. If drinking stops this process reverses in around 2 weeks.
  2. Alcoholic hepatitis Drinking alcohol over a long period causes inflammation in the liver sites. Binge drinking is associated with the same effect. Mild alcoholic hepatitis is usually reversible with permanent abstinence.
  3. Cirrhosis Scar tissue replaces normal tissue. Irreversible. Stopping drinking can prevent further damage. Continued drinking has v poor prognosis.
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2
Q

Treatment of non alcoholic fatty liver disease

A

Mainstay is gradual weight loss (0.5-1 kg/wk) as rapid weight loss can worsen liver disease. Aim to lose at least 7-10% of body weight • some evidence for vitamin E (800 U daily) if there is hepatic inflammation • some evidence for benefits of coffee drinking (3 cups/d) and vitamin D Pioglitazone

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3
Q

Deranged AST and ALT suggests what?

A

Hepatocellular injury

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4
Q

Deranged ALP and bilirubin suggests what?

A

Cholestasis

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5
Q

Features of Wernicke’s encephalopathy

A

Confusion Oculomotor disturbances (disturbances of eye movements) Ataxia (difficulties with coordinated movements)

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6
Q

Stages of non-alcoholic fatty liver disease

A
  1. Non-alcoholic Fatty Liver Disease
  2. Non-Alcoholic Steatohepatitis (NASH)
  3. Fibrosis
  4. Cirrhosis
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7
Q

Risk factors non alcoholic fatty liver disease

A

Obesity Poor diet and low activity levels Type 2 diabetes High cholesterol Middle age onwards Smoking High blood pressure

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8
Q

Gold standard for diagnosis of cirrhosis

A

Liver biopsy Show bridging fibrosis and nodular regeneration

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9
Q

Progress of lab abnormalities in cirrhosis

A

Fall in platelet count <150 is the earliest finding, followed many years later with rise in INR, fall in albumin, rise in bilirubin, fall in glucose level (pre-terminal event)

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10
Q

Signs of cirrhosis

A
  • Jaundice – caused by raised bilirubin
  • Hepatomegaly – however the liver can shrink as it becomes more cirrhotic
  • Splenomegaly – due to portal hypertension
  • Spider Naevi – these are telangiectasia with a central arteriole and small vessels radiating away
  • Palmar Erythema – caused by hyperdynamic cirulation
  • Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
  • Bruising – due to abnormal clotting
  • Ascites
  • Caput Medusae – distended paraumbilical veins due to portal hypertension
  • Asterixis – “flapping tremor” in decompensated liver disease
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11
Q

What is the MELD score in cirrhosis?

A

• Predicts 3 mo survival and used to stratify patients on transplant list • Based on creatinine, INR, total bilirubin, and serum sodium concentration

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12
Q

General management of cirrhosis patients

A
  • Ultrasound and alpha-fetoprotein every 6 months for hepatocellular carcinoma
  • Endoscopy every 3 years in patients without known varices
  • High protein, low sodium diet
  • MELD score every 6 months
  • Consideration of a liver transplant
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13
Q

Management of ascites

A

-Sodium restriction -Diuretics (frusemide + spironolactone) -Prophylactic antibiotics against spontaneous bacterial peritonitis -Large volume paracentesis -TIPS

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14
Q

What can present with fever, abdominal pain, vomiting chills and nausea in a cirrhosis patient?

A

Spontaneous bacterial peritonitis. V bad prognosis

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15
Q

The mechanism for the development of ascites

A

Ascites is fluid in the peritoneal cavity. Increased pressure in the portal system causes fluid to leak from capillaries in the liver and bowel and in to the peritoneal cavity. The drop in circulating volume caused by fluid loss into the peritoneal space causes a reduction in blood pressure entering the kidneys. The kidneys sense this lower pressure and release renin, which leads to increased aldosterone secretion (via the renin-angiotensin-aldosterone system) and reabsorption of fluid and sodium in the kidneys. Cirrhosis causes a transudative, meaning low protein content, ascites. Ascites marks the start of decompensated liver disease.

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16
Q

Management of spontaneous bacterial peritonitis.

A

Take an ascitic culture prior to giving antibiotics Usually treated with an IV cephalosporin such as cefotaxime

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17
Q

Sites of varices

A

Gastro oesophageal junction

Ileocaecal junction

Rectum

Anterior abdominal wall via the umbilical vein (caput medusae

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18
Q

Treatment of stable varices

A
  • Propranolol reduces portal hypertension by acting as a non-selective beta blocker
  • Elastic band ligation of varices
  • Injection of sclerosant (less effective than band ligation)
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19
Q

Treatment of bleeding oesophageal varices

A
  • Resuscitation
  • Vasopressin analogues (i.e. terlipressin) cause vasoconstriction + slow bleeding in varices
  • Correct any coagulopathy with vitamin K + FFP (which is full of clotting factors)
  • Giving prophylactic broad spectrum antibiotics has been shown to reduce mortality
  • Consider intubation and intensive care as they can bleed very quickly and become life threateningly unwell
  • Urgent endoscopy
  • Injection of sclerosant into varices can be used to cause “inflammatory obliteration” of vessel
  • Elastic band ligation of varices
  • Sengstaken-Blakemore Tube = inflatable tube inserted into the oesophagus to tamponade bleeding varices. Used when endoscopy fails.
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20
Q

Most useful lab test to diagnose hepatic encephalopathy

A

Ammonia

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21
Q

Mode of inheritance, gene and chromosome for Wilson’s disease

A

Autosomal recessive defect in copper elimination (gene ATP7B) chromosome 13

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22
Q

Typical bacteria in spontaneous bacterial peritonitis

A

Gram-negatives compose 70% of pathogens: E. coli (most common), Streptococcus, Klebsiella

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23
Q

Copper deposition in the liver leads to what?

A

Chronic hepatitis and eventually liver cirrhosis

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24
Q

In Wilson’s disease copper deposits in the brain lead to what?

A

Deposits in the basal ganglia lead to Parkinsonism

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25
Eye sign in Wilson's disease + proper method of examination
Kayser-Fleischer rings in cornea (deposition of copper in Descemet’s corneal membrane) Examine via slit lamp
26
Initial investigation of choice in Wilson's disease
Serum caeruloplasmin. May be low in Wilson's Note it's not specific and can be affected by cancer or inflammatory conditions
27
The definitive gold standard test for diagnosis Wilson's disease
Liver biopsy for liver copper content
28
Rx Wilson's disease
Copper chelation using: * Penicillamine * Trientene
29
Liver biopsy showing acid-Schiff-positive staining globules in hepatocytes is associated with what?
Alpha-1 antitrypsin
30
Liver biopsy with Perl’s stain to diagnose what?
Haemochromatosis
31
Haemochromatosis complications
* Type 1 Diabetes * Liver Cirrhosis * Iron deposits in the pituitary and gonads lead to endocrine and sexual problems (hypogonadism, impotence, amenorrhea, infertility) * Cardiomyopathy (iron deposits in the heart) * Hepatocellular Carcinoma * Hypothyroidism (iron deposits in the thyroid) * Chrondocalcinosis / pseudogout (calcium deposits in joints) causing arthritis
32
An antibody specific to primary biliary cirrhosis which forms part of the diagnostic criteria
Anti-mitochondrial antibodies
33
Investigation to confirm diagnosis of primary biliary cirrhosis
Liver biopsy
34
Who gets primary biliary cirrhosis?
mainly middle-aged women (M:F = 1:9)
35
Antibodies in coeliac disease
* Anti-tissue transglutaminase (anti-TTG) * Anti-endomysial (anti-EMA). * Also Deaminated gliadin peptides antibodies (anti-DGPs) These antibodies relate to disease activity and will rise with more active disease and may disappear with effective treatment.
36
Basic pathological process in coeliac disease
Auto-antibodies are created in response to exposure to gluten that target the epithelial cells of the intestine and lead to inflammation
37
Genetic associations of coeliac disease
HLA-DQ2 gene (90%) HLA-DQ8 gene
38
What should you also test for when you test for anti-TTG and anti-EMA antibodies in coeliac disease?
It is important to test for total Immunoglobulin A levels because if total IgA is low because they have an IgA deficiency then the coeliac test will be negative even when they have coeliac
39
Coeliac disease associations
* Type 1 Diabetes * Thyroid disease * Autoimmune hepatitis * Primary biliary cirrhosis * Primary sclerosing cholangitis
40
Complications of Untreated Coeliac Disease
* Vitamin deficiency * Anaemia * Osteoporosis * Ulcerative jejunitis * Enteropathy-associated T-cell lymphoma (EATL) of the intestine * Non-Hodgkin lymphoma (NHL) * Small bowel adenocarcinoma (rare)
41
Endoscopy and intestinal biopsy in Coeliac disease show:
Crypt hypertrophy Villous atrophy
42
Rapid urease test (CLO test) is for what?
H pylori, on endoscopy
43
Causes of upper GI bleeding
* Oesophageal varices * Mallory-Weiss tear, which is a tear of the oesophageal mucous membrane * Ulcers of the stomach or duodenum * Cancers of the stomach or duodenum
44
Difference in inflammation histopathologically between UC and Crohns
**UC**- mucosa and submucosa only, always involving the rectum and extends proximally continuously **Crohns**- patchy inflammation with skip lesions, can be transmural and even cause fistulas with other organs
45
Bloody diarrhoea- Crohns or UC?
UC. Which remember is always in the rectum
46
Worse risk of cancer- Crohns or UC?
UC. Marked increase in risk esp colorectal.
47
What do you not do if you think someone has a toxic megacolon?
Any kind of tube or scope
48
Fistulas- Crohns or UC?
Crohns. Always.
49
Iron deficiency anaemia in an elderly patient is what until proven otherwise?
Colorectal carcinoma
50
Risk factors colorectal cancer
* Age * Hereditary polyposis syndromes * Family history IBD (UC more than Crohns) * Adenomatous polyps * Low fibre high fat diet
51
Colorectal cancer staging is based on what?
Degree of penetration through bowel wall + lymph nodes + mets This is the TNM classification
52
Tubular vs villous colorectal polyps- which are worse?
Villous
53
Definition of portal hypertension
pressure gradient between hepatic vein pressure and wedged hepatic vein pressure (corrected sinusoidal pressure) \>5 mmHg
54
Treatment of portal hypertension
* non-selective Beta-blockers (propanolol, nadolol, carvedilol) decrease risk of bleeding from varices * TIPS: to decrease portal venous pressure radiologically inserted stent between portal and hepatic vein via transjugular vein catheterization and percutaneous puncture of portal vein can be used to stop acute bleeding or prevent rebleeding or treat ascites complications: hepatic encephalopathy, deterioration of hepatic function -contraindicated with severe liver dysfunction, -uncontrolled hepatic encephalopathy, and congestive heart failure -most commonly used as a “bridge” to liver transplant
55
Causes of acute pancreatitis
GET SMASHED * Gallstones (45%) * Ethanol (35%) * Tumours: pancreas, ampulla, choledochocele * Scorpion stings * Microbiological bacterial: Mycoplasma, Campylobacter, TB, M. avium intracellulare, Legionella, leptospirosis viral: mumps, rubella, varicella, viral hepatitis, CMV, EBV, HIV, Coxsackie virus, echovirus, adenovirus parasites: ascariasis, clonorchiasis, echinococcosis * Autoimmune: SLE, polyarteritis nodosa (PAN), Crohn’s disease * Surgery/trauma manipulation of sphincter of Oddi (e.g. ERCP), post-cardiac surgery, blunt trauma to abdomen, penetrating peptic ulcer * Hyperlipidemia (TG \>11.3 mmol/L; \>1000 mg/dL), hypercalcemia, hypothermia * Emboli or ischemia * Drugs/toxins azathioprine, mercaptopurine, furosemide, estrogens, methyldopa, H2-blockers, valproic acid,
56
What is Cullen's sign
Periumbilical ecchymosis
57
What is Grey Turner sign?
Flank bruising
58
Complications of acute pancreatitis
* Pancreatic pseudocyst * Fistula formation * Hypocalcemia * Renal failure * Pleural effusion * Chronic pancreatitis * Sepsis * ARDS
59
Complications of chronic pancreatitis
Chronic pain Diabetes Malnutrition/ weight loss Splenic vein thrombosis Pancreatic cancer
60
75% of pancreatic cancers are what type?
Adenocarcinomas in the head of the pancreas
61
Risk factors for pancreatic cancer
* Smoking * Chronic pancreatitis * First degree relative
62
Best initial test for pancreatic cancer
CT
63
Surgical procedure for pancreatic cancer
Whipple's procedure (pancreaticoduodenectomy)
64
Is there an increased prevalence of irritable bowel syndrome after infectious enteritis?
Yes According to Canada Q Bank
65
Antipruritic agents
* Cholestyramine * Rifampicin * Antihistamines * Plasmapheresis
66
Middle aged women presenting with intense itch, hepatomegaly and Sjogren's syndrome
Primary biliary cholangitis
67
The main medication used to slow the progression of primary biliary cholangitis
Ursodiol
68
Predisposing factors for sigmoid volvulus
* Age * Constipation * Bed bound Institutionalised patients with neuropsychiatric disorders * Psychotropic drug use * High fibre diet
69
The lab abnormality most sensitive for pancreatitis
Lipase Highly specific if it is elevated three fold
70
By how much does Barrett's esophagus increase the risk of cancer? And how often should you screen for it? What determines how often you should screen?
40-fold so screen 3-5 yearly if there is no dysplasia 6-12 monthly low grade dysplasia 3 monthly high grade dysplasia
71
Best investigation for RUQ pain
Ultrasonography
72
Rx for severe rectal pain eg radiation proctitis
Sucralfate or glucocorticoid enema
73
Bronze diabetes- Type I DM plus hyper pigmented skin- what is this?
Haemochromatosis
74
Name an iron chelator
Deferasirox
75
Best diagnostic test for primary sclerosing cholangitis
MRCP Magnetic resonance cholangiopancreatography
76
Ranson's criteria are for what?
Risk of mortality in pancreatitis
77
Usual cause of isolated hyperbilirubunemia in an otherwise healthy young man
Gilbert's syndrome It's unconjugated
78
In alcoholic pancreatitis amylase levels are less likely to be elevated, true or false
True
79
Treatment of choice for fistulating Crohn's disease
Anti-TNF drugs like Infliximab
80
Lab test which best prognostic indicator in primary biliary cholangitis
Serum bilirubin
81
Causes of rectal bleeding
* Hemorrhoids * Anal fissure * Colon or rectal cancer * Proctitis or IBD or colitis * Diverticulosis
82
Classical signs of oesophageal perforation (Boerhaave syndrome)
Boerhaave syndrome is spontaneous rupture of the oesophagus and is associated w epigastric pain, epigastric guarding, and classically subcutaneous emphysema of the suprasternal notch \*\*\*
83
Courvoisier's sign
Palpable, non-tender gallbladder- suggests pancreatic cancer
84
Most likely cause of acute lower GI bleed in pts \> 40
Diverticulosis
85
Difference between Mallory Weiss and Boerhaave tears
Boerhaave is full thickness esophageal rupture
86
Grey Turner and Cullen's sign Pancreatitis
87
Kayser-Fleischer rings Wilson's disease
88
Clinical signs of decompensated cirrhosis. 1. Jaundice 2. Ascites 3. Splenomegaly 4. Digital clubbing

MCCQE1 (20 decks)

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