Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Deranged AST and ALT suggests what?

A

Hepatocellular injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Deranged ALP and bilirubin suggests what?

A

Cholestasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Features of Wernicke’s encephalopathy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Gold standard for diagnosis of cirrhosis

A

Liver biopsy Show bridging fibrosis and nodular regeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Management of ascites

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

Spontaneous bacterial peritonitis. V bad prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Sites of varices

A

Gastro oesophageal junction

Ileocaecal junction

Rectum

Anterior abdominal wall via the umbilical vein (caput medusae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Most useful lab test to diagnose hepatic encephalopathy

A

Ammonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Typical bacteria in spontaneous bacterial peritonitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Copper deposition in the liver leads to what?

A

Chronic hepatitis and eventually liver cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A

Deposits in the basal ganglia lead to Parkinsonism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Eye sign in Wilson’s disease + proper method of examination

A

Kayser-Fleischer rings in cornea (deposition of copper in Descemet’s corneal membrane)

Examine via slit lamp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Initial investigation of choice in Wilson’s disease

A

Serum caeruloplasmin.

May be low in Wilson’s Note it’s not specific and can be affected by cancer or inflammatory conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

The definitive gold standard test for diagnosis Wilson’s disease

A

Liver biopsy for liver copper content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Rx Wilson’s disease

A

Copper chelation using:

  • Penicillamine
  • Trientene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Liver biopsy showing acid-Schiff-positive staining globules in hepatocytes is associated with what?

A

Alpha-1 antitrypsin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Liver biopsy with Perl’s stain to diagnose what?

A

Haemochromatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Haemochromatosis complications

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

An antibody specific to primary biliary cirrhosis which forms part of the diagnostic criteria

A

Anti-mitochondrial antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Investigation to confirm diagnosis of primary biliary cirrhosis

A

Liver biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Who gets primary biliary cirrhosis?

A

mainly middle-aged women (M:F = 1:9)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Antibodies in coeliac disease

A
  • 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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Basic pathological process in coeliac disease

A

Auto-antibodies are created in response to exposure to gluten that target the epithelial cells of the intestine and lead to inflammation

37
Q

Genetic associations of coeliac disease

A

HLA-DQ2 gene (90%) HLA-DQ8 gene

38
Q

What should you also test for when you test for anti-TTG and anti-EMA antibodies in coeliac disease?

A

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
Q

Coeliac disease associations

A
  • Type 1 Diabetes
  • Thyroid disease
  • Autoimmune hepatitis
  • Primary biliary cirrhosis
  • Primary sclerosing cholangitis
40
Q

Complications of Untreated Coeliac Disease

A
  • Vitamin deficiency
  • Anaemia
  • Osteoporosis
  • Ulcerative jejunitis
  • Enteropathy-associated T-cell lymphoma (EATL) of the intestine
  • Non-Hodgkin lymphoma (NHL)
  • Small bowel adenocarcinoma (rare)
41
Q

Endoscopy and intestinal biopsy in Coeliac disease show:

A

Crypt hypertrophy Villous atrophy

42
Q

Rapid urease test (CLO test) is for what?

A

H pylori, on endoscopy

43
Q

Causes of upper GI bleeding

A
  • 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
Q

Difference in inflammation histopathologically between UC and Crohns

A

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
Q

Bloody diarrhoea- Crohns or UC?

A

UC. Which remember is always in the rectum

46
Q

Worse risk of cancer- Crohns or UC?

A

UC. Marked increase in risk esp colorectal.

47
Q

What do you not do if you think someone has a toxic megacolon?

A

Any kind of tube or scope

48
Q

Fistulas- Crohns or UC?

A

Crohns. Always.

49
Q

Iron deficiency anaemia in an elderly patient is what until proven otherwise?

A

Colorectal carcinoma

50
Q

Risk factors colorectal cancer

A
  • Age
  • Hereditary polyposis syndromes
  • Family history IBD (UC more than Crohns)
  • Adenomatous polyps
  • Low fibre high fat diet
51
Q

Colorectal cancer staging is based on what?

A

Degree of penetration through bowel wall + lymph nodes + mets This is the TNM classification

52
Q

Tubular vs villous colorectal polyps- which are worse?

A

Villous

53
Q

Definition of portal hypertension

A

pressure gradient between hepatic vein pressure and wedged hepatic vein pressure (corrected sinusoidal pressure) >5 mmHg

54
Q

Treatment of portal hypertension

A
  • 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
Q

Causes of acute pancreatitis

A

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
Q

What is Cullen’s sign

A

Periumbilical ecchymosis

57
Q

What is Grey Turner sign?

A

Flank bruising

58
Q

Complications of acute pancreatitis

A
  • Pancreatic pseudocyst
  • Fistula formation
  • Hypocalcemia
  • Renal failure
  • Pleural effusion
  • Chronic pancreatitis
  • Sepsis
  • ARDS
59
Q

Complications of chronic pancreatitis

A

Chronic pain Diabetes Malnutrition/ weight loss Splenic vein thrombosis Pancreatic cancer

60
Q

75% of pancreatic cancers are what type?

A

Adenocarcinomas in the head of the pancreas

61
Q

Risk factors for pancreatic cancer

A
  • Smoking
  • Chronic pancreatitis
  • First degree relative
62
Q

Best initial test for pancreatic cancer

A

CT

63
Q

Surgical procedure for pancreatic cancer

A

Whipple’s procedure (pancreaticoduodenectomy)

64
Q

Is there an increased prevalence of irritable bowel syndrome after infectious enteritis?

A

Yes According to Canada Q Bank

65
Q

Antipruritic agents

A
  • Cholestyramine
  • Rifampicin
  • Antihistamines
  • Plasmapheresis
66
Q

Middle aged women presenting with intense itch, hepatomegaly and Sjogren’s syndrome

A

Primary biliary cholangitis

67
Q

The main medication used to slow the progression of primary biliary cholangitis

A

Ursodiol

68
Q

Predisposing factors for sigmoid volvulus

A
  • Age
  • Constipation
  • Bed bound Institutionalised patients with neuropsychiatric disorders
  • Psychotropic drug use
  • High fibre diet
69
Q

The lab abnormality most sensitive for pancreatitis

A

Lipase Highly specific if it is elevated three fold

70
Q

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?

A

40-fold so screen 3-5 yearly if there is no dysplasia 6-12 monthly low grade dysplasia 3 monthly high grade dysplasia

71
Q

Best investigation for RUQ pain

A

Ultrasonography

72
Q

Rx for severe rectal pain eg radiation proctitis

A

Sucralfate or glucocorticoid enema

73
Q

Bronze diabetes- Type I DM plus hyper pigmented skin- what is this?

A

Haemochromatosis

74
Q

Name an iron chelator

A

Deferasirox

75
Q

Best diagnostic test for primary sclerosing cholangitis

A

MRCP Magnetic resonance cholangiopancreatography

76
Q

Ranson’s criteria are for what?

A

Risk of mortality in pancreatitis

77
Q

Usual cause of isolated hyperbilirubunemia in an otherwise healthy young man

A

Gilbert’s syndrome It’s unconjugated

78
Q

In alcoholic pancreatitis amylase levels are less likely to be elevated, true or false

A

True

79
Q

Treatment of choice for fistulating Crohn’s disease

A

Anti-TNF drugs like Infliximab

80
Q

Lab test which best prognostic indicator in primary biliary cholangitis

A

Serum bilirubin

81
Q

Causes of rectal bleeding

A
  • Hemorrhoids
  • Anal fissure
  • Colon or rectal cancer
  • Proctitis or IBD or colitis
  • Diverticulosis
82
Q

Classical signs of oesophageal perforation (Boerhaave syndrome)

A

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
Q

Courvoisier’s sign

A

Palpable, non-tender gallbladder- suggests pancreatic cancer

84
Q

Most likely cause of acute lower GI bleed in pts > 40

A

Diverticulosis

85
Q

Difference between Mallory Weiss and Boerhaave tears

A

Boerhaave is full thickness esophageal rupture

86
Q
A

Grey Turner and Cullen’s sign

Pancreatitis

87
Q
A

Kayser-Fleischer rings

Wilson’s disease

88
Q
A

Clinical signs of decompensated cirrhosis.

  1. Jaundice
  2. Ascites
  3. Splenomegaly
  4. Digital clubbing

MCCQE1 (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions