Brainscape's Knowledge GenomeTM

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


See full index

FINALS > GASTROENTEROLOGY > Flashcards

GASTROENTEROLOGY Flashcards

1
Q

What are the features of Wernicke’s encephalopathy?

A 
CAN OPEN:
Confusion
Ataxia
Nystagmus
Ophthamoplegia
PEripheral 
Neuropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the antibiotic management of C.diff infection?

A
  1. Oral vancomycin
  2. Oral fidaxomicin
  3. Oral vancomycin + IV metronidazole

Life-threatening = oral vancomycin AND IV metronidazole

Recurrent = oral fidaxomicin (<12 weeks) + oral vancomycin (>12 weeks)

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

Which antibiotics are associated with c.diff infection?

A

Second & third gen cephalosporins (ceftriaxone)
Clindamycin

+ PPIs

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

Which marker is used to determine the severity of c.diff infection?

A

WCC
<15 = moderate
>15 = severe

Hypotension/toxic megacolon = life-threatening

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

How is C.diff infection diagnosed?

A

CDT (C.diff toxin) in the stool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name 5 causes of hepatitis?

A 
• Alcoholic hepatitis
• Non alcoholic fatty liver disease
• Viral hepatitis
• Autoimmune hepatitis
- Drug induced hepatitis (e.g. paracetamol overdose)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does hepatitis present?

A 
• Abdominal pain
• Fatigue
• Pruritis (itching)
• Muscle and joint aches
• Nausea and vomiting
• Jaundice 
Fever (viral hepatitis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is found on liver function tests in hepatitis?

A

^AST/ALT
^ALP (but less rise)
Bilirubin^

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the most common viral hepatitis worldwide?

A

A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which viral hepatitis’ can you receive vaccinations for?

A

A, B (notifiable diseases PHE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is hepatitis A transmitted?

A

Faecal oral (contaminated warer/food)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does hepatitis A present?

A 
Nausea
Vomiting
Anorexia
Jaundice
Cholestasis - pale stools, dark urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the management of hepatitis A?

A

Analgesia
Resolves without treatment 1-3 months
Notify PHE

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

What causes hepatitis B?

A

DNA virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is hepatitis B transmitted?

A

Sex
IVDU
Tattoos
Vertical transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How long is recovery from hepatitis B?

A

2-3 months

Some people are carriers for life

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

What is implied by E antigen on hepatitis serology (HBeAg)?

A

High infectivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is HBV DNA?

A

Direct count of viral load of hepatitis B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How can you confirm a response to the hepatitis B vaccine?

A

HBsAg (surface antigen)

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

What is the management of hepatitis B?

A 
Refer to gastroenterology for specialist management
Education about reducing transmission
Antivirals
Liver transplantation (end stage)
Notify PHE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What causes hepatitis C?

A

RNA virus

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

What is the transmission of hepatitis C?

A

Blood/bodily fluids

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

What is the prognosis for hepatitis C?

A

1/4 full recovery

3/4 chronic disease –> liver cirrhosis –> hepatocellular carcinoma

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

How can you test for hepatitis C?

A

Hepatitis C RNA testing

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

What is the management for hepatitis C?

A 
Refer to gastroenterology for specialist management
Education about reducing transmission
Direct acting antivirals (curative)
Liver transplantation (end stage)
Notify PHE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What causes hepatitis D?

A

RNA virus

Can only be concomitant with hepatitis B

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

What is the management of hepatitis D?

A

No specific treatment

Notify PHE

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

What causes hepatitis E?

A

RNA virus

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

How is hepatitis E transmitted?

A

Faecal oral route

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

How does hepatitis E present?

A

Mild illness
No treatment required
Cleared within a month
Rarely causes chronic hepatitis in immunocompromised patients

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

What are the two types of autoimmune hepatitis?

A

Type 1: occurs in adults

Type 2: occurs in children

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

How does type 1 autoimmune hepatitis present?

A

Type 1 typically affects women in their late forties or fifties. It presents around or after the menopause with fatigue and features of liver disease on examination. It takes a less acute course than type 2.

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

How does type 2 autoimmune hepatitis present?

A

In type 2, patients in their teenage or early twenties present with acute hepatitis with high transaminases and jaundice.

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

Which antibodies are found in type 1 autoimmune hepatitis?

A

• Anti-nuclear antibodies (ANA)
• Anti-smooth muscle antibodies (anti-actin)
Anti-soluble liver antigen (anti-SLA/LP)

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

Which antibodies are found in type 2 autoimmune hepatitis?

A

• Anti-liver kidney microsomes-1 (anti-LKM1)

Anti-liver cytosol antigen type 1 (anti-LC1)

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

How is autoimmune hepatitis diagnosed?

A

Liver biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the management of autoimmune hepatitis?

A
  1. High dose steroids (prednisolone)

2. Introduce immunosuppressants - azathioprine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How do you screen for harmful alcohol use?

A

CAGE questionnaire

C - cut down?
A - annoyed about other people saying you should cut down
G - guilty about your drinking?
E - eye opener

OR

AUDIT questionnaire (10 questions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the complications of harmful alcohol use?

A 
• Alcoholic Liver Disease
• Cirrhosis and the complications of cirrhosis including hepatocellular carcinoma
• Alcohol Dependence and Withdrawal
• Wernicke-Korsakoff Syndrome (WKS)
• Pancreatitis
Alcoholic Cardiomyopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the features of Wernicke’s encephalopathy?

A
  1. Confusion
  2. Oculomotor disturbances (disturbances of eye movements)
  3. Ataxia (difficulties with coordinated movements)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the features of Korsakoff’s syndrome?

A 
Memory impairment (retrograde and anterograde)
Behavioural changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the management of Wernicke’s encephalopathy?

A

Pabrinex (high dose vitamin B - thiamine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Name 4 causes of Wernicke’s encephalopathy?

A

Alcohol excess
Persistent vomiting
Stomach cancer
Dietary deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the symptoms of alcohol withdrawal?

A

6-12 hours: tremor, sweating, headache, craving and anxiety
12-24 hours: hallucinations
24-48 hours: seizures
24-72 hours: “delirium tremens”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is the mortality of DTs?

A

35%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the first-line treatment of DTs?

A

Lorazepam PO

IV lorazepam or haloperidol
If DT develops during detox, review regimen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What scoring system is used to assess alcohol withdrawal?

A

The CIWA-Ar (Clinical Institute Withdrawal Assessment – Alcohol revised) tool can be used to score the patient on their withdrawal symptoms and guide treatment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the first-line treatment for alcohol withdrawal?

A

Chlordiazepoxide (librium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the management of alcohol withdrawal?

A

Chlordiazepoxide

IV high dose vitamin B (pabrinex) (followed by regular dose thiamine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is used to detox from alcohol?

A

Chlordiazepoxide - either fixed or variable dose depending on symptoms
Preferably done as an inpatient to manage side effects and precent DTs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What medications can be used to prevent relapse in alcohol addiction?

A 
• Group therapy or self-help (e.g. AA) 
• Naltrexone - decrease the amount and frequency of drinking (DO NOT use with opioids = may precipitate withdrawal)
• Baclofen: ↓ cravings 
• Acamprosate: ↓ cravings 
Disulfiram: aversion therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are the three steps in the progression of alcoholic liver disease?

A
  1. Alcohol related fatty liver disease
  2. Alcoholic hepatitis
    Cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the signs of liver disease?

A 
• Jaundice
• Hepatomegaly
• Spider Naevi
• Palmar Erythema
• Gynaecomastia
• Bruising – due to abnormal clotting
• Ascites
• Caput Medusae – engorged superficial epigastric veins
Asterixis – “flapping tremor” in decompensated liver disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What bloods should be checked in alcoholic liver disease?

A 
FBC = MCV
LFT = AST>ALT, gamma-GT^
Clotting = PT^
U&Es = hepatorenal syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the treatment of alcoholic hepatitis?

A

Steroids improve short term outcomes (over 1 month)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Which score is used to determine the need for steroid therapy and severity of alcoholic hepatitis? What is the cut off score?

A

Maddrey Discriminant Function

Score >32 = steroid therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Which score predicts mortality in alcoholic hepatitis?

A

Glasgow alcoholic hepatitis score

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the management of alcoholic cirrhosis?

A

Treat complications of cirrhosis (portal hypertension, varices, ascites and hepatic encephalopathy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the definitive treatment of alcoholic cirrhosis?

A

Referral for liver transplant in severe disease however they must abstain from alcohol for 3 months prior to referral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Which score is used to determine the severity of liver cirrhosis? Which values are used to calculate this score?

A

MELD - uses a combination of INR, BR and creatinine to determine survival and severity of cirrhosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Which scoring systems is used for the prognosis of chronic liver disease?

A

Child-Pugh score

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Which score is used in ED and primary care to determine the need for further alcohol screening?

A

FAST

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

How does alcoholic ketoacidosis present?

A

Abdominal pain

Vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What might be seen on an ABG in alcoholic ketoacidosis?

A

Normal glucose
^Ketones
Metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Who is at risk of developing alcoholic ketoacidosis?

A

Chronic binge drinkers, especially if not eating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is the treatment of alcohol ketoacidosis?

A

IV fluids

Thiamine (vit B1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is PBC?

A

immune system attacks the small bile ducts within the liver

Causes obstruction of bile –> cholestasis –> fibrosis –> cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Which part of the liver is affected first in PBC?

A

Intralobar ducts, also known as the Canals of Hering.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Which three liver products build up in the blood due to PBC and cause symptoms?

A

Bile acids - pruritis
Bilirubin - jaundice
Cholesterol - xanthelasma (+ increase risk of cardiovascular disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the role of bile acids?

A

Digestion of fats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the risk factors for PBC?

A
  • Middle aged women
  • Other autoimmune diseases (e.g. thyroid, coeliac)
  • Rheumatoid conditions (e.g. systemic sclerosis, Sjogrens and rheumatoid arthritis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

How does PBC present?

A 
• Fatigue
• Pruritus
• GI disturbance and abdominal pain
• Jaundice
• Pale stools
• Xanthoma and xanthelasma
Signs of cirrhosis and failure (e.g. ascites, splenomegaly, spider naevi)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

How is PBC diagnosed and staged?

A

Liver biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Which liver enzyme is raised first in PBC and PSC?

A

ALP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Which autoantibodies are found in PBC? Which is most specific?

A

AMA - most specific (part of the diagnostic criteria)

ANA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Which blood tests are done in suspected PBC?

A

LFTs
Antibodies - ANA, AMA
ESR - raised
IgM - raised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the treatment of PBC? (4)

A

• Ursodeoxycholic acid reduces the intestinal absorption of cholesterol
• Colestyramine is a bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids
• Liver transplant in end stage liver disease
Immunosuppression (e.g. with steroids) is considered in some patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the action of ursodeoxycholic acid?

A

reduces the intestinal absorption of cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is the action of colesyramine?

A

bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is the definitive management of PBC?

A

Liver transplant in end stage liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is PSC?

A

intrahepatic or extrahepatic ducts become strictured and fibrotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is the cause of PSC?

A

Unclear

Genetic
Autoimmune
Ulcerative colitis (70%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What are the risk factors for PSC?

A

• Male
• Aged 30-40
• Ulcerative Colitis
Family History

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

How does PSC present?

A 
• Jaundice
• Chronic right upper quadrant pain
• Pruritus
• Fatigue
Hepatomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is the role of autoantibody testing in PSC?

A

Limited
Antibodies are non-specific
Might indicate whether there will be a response to immunosuppressants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Which autoantibodies are associated with PSC?

A

• Antineutrophil cytoplasmic antibody (p-ANCA) in up to 94%
• Antinuclear antibodies (ANA) in up to 77%
Anticardiolipin antibodies (aCL) in up to 63%

87
Q

What is the gold standard diagnostic investigation in PSC?

A

MRCP

88
Q

What is the management of PSC?

A

Liver transplant (80% 5 year survival)
ERCP - dilate & stent
Colestyramine - bile acid sequestrate
Monitoring for complications

89
Q

What are the complications of PSC?

A 
• Acute bacterial cholangitis
• Cholangiocarcinoma develops in 10-20% of cases
• Colorectal cancer
• Cirrhosis and liver failure
• Biliary strictures
Fat soluble vitamin deficiencies
90
Q

What are the four most common causes of cirrhosis?

A

• Alcoholic liver disease
• Non Alcoholic Fatty Liver Disease
• Hepatitis B
Hepatitis C

91
Q

Give some 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 circulation
• 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

92
Q

Why do you get gynaecomastia in liver cirrhosis?

A

Endocrine dysfunction:
increased production of androstenedione by the adrenal glands
increased aromatisation of androstenedione to oestrogen loss of clearance of adrenal androgens by the liver

93
Q

What is seen on LFTs in cirrhosis?

A

May be normal

Decompensated = all markers deranged

94
Q

What is first-line investigation for assessing fibrosis in non-alcoholic fatty liver disease?

A

Enhanced Liver Fibrosis (ELF) blood test

95
Q

How is the ELF blood test interpreted?

A 
• Nodularity of the surface of the liver
• A “corkscrew” appearance to the arteries with increased flow as they compensate for reduced portal flow
• Enlarged portal vein with reduced flow
• Ascites
Splenomegaly
96
Q

When should you screen for hepatocellular carcinoma in cirrhosis? What does screening involve?

A

US and alpha-fetoprotein

Every 6 months

97
Q

What is a Fibroscan?

A

Checks the elasticity of the liver

Assesses the degree of cirrhosis

98
Q

Which patients should receive a Fibroscan?

A

Every 2 years in patients at risk of cirrhosis:
• Hepatitis C
• Heavy alcohol drinkers (men drinking > 50 units or women drinking > 35 units per week)
• Diagnosed alcoholic liver disease
• Non alcoholic fatty liver disease and evidence of fibrosis on the ELF blood test
Chronic hep B (every year)

99
Q

Which three markers are measured by ELF blood test?

A

HA, PIIINP and TIMP-1

100
Q

Which scoring systems can be used to assess prognosis of cirrhosis?

A

Child-Pugh Score

MELD score

101
Q

Which markers are used in the MELD score? (5)

A 
Bilirubin
Creatinine
INR
Sodium
Dialysis
102
Q

How is the MELD score used?

A

gives a percentage estimated 3 month mortality and helps guide referral for liver transplant

103
Q

When should patients with cirrhosis get a MELD score?

A

Every 6 months

104
Q

What is the general management of cirrhosis?

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
105
Q

What is the 5 year survival of cirrhosis?

A

50%

106
Q

Name 6 complications of cirrhosis.

A 
Malnutrition
Portal hypertension & varices 
Ascites & SBP
Hepatic encephalopathy
Hepatorenal syndrome
HCC
107
Q

How does cirrhosis lead to muscle wasting?

A

increased use of muscle tissue as fuel and reduces the protein available in the body for muscle growth

108
Q

What advice can you give to avoid malnutrition in cirrhosis?

A

• Regular meals (every 2-3 hours)
• Low sodium (to minimise fluid retention)
• High protein and high calorie (particularly if underweight)
Avoid alcohol

109
Q

How does cirrhosis lead to portal hypertension?

A

Scarring of the liver increases resistance to blood flow

Pressure builds in portal system

110
Q

Where do varices most commonly occur?

A
  • Gastro oesophageal junction
  • Ileocaecal junction
  • Rectum
  • Anterior abdominal wall via the umbilical vein (caput medusae)
111
Q

How do you treat 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)

112
Q

What can be done if the medical and endoscopic treatment of varices fails?

A

TIPS procedure

113
Q

What is ascites?

A

Fluid accumulation within the abdomen.

114
Q

What is the pathophysiology of ascites?

A

Portal HTN causes leaking of fluid from capillaries in the liver/bowel into the peritoneal cavity.
Loss of circulating volume causes the kidneys to produce renin –> aldosterone.
Aldosterone leads to increased reabsorption of fluid and sodium.

115
Q

What type of ascites is caused by cirrhosis?

A

Transudative (low protein) - HIGH SAAG

116
Q

What is SAAG? How is it used and how is it calculated?

A

SAAG = serum-ascites albumin gradient
It is used to determined the cause of ascites.
SAAG = (serum albumin concentration) - (ascitic albumin concentration)

117
Q

How can the causes of ascites be grouped?

A 
High SAAG (>11g/L)
Low SAAG (<11g/L)
118
Q

What are the high SAAG causes of ascites?

A

Liver disease - acute liver failure, cirrhosis, liver metastases = PORTAL HTN
Cardiac - RHF, constrictive pericarditis
Other - Budd-Chiari syndrome, portal vein thrombosis

119
Q

What are the low SAAG causes of ascites?

A

Nephrotic syndrome
Peritoneal carcinoma
Infection - TB

120
Q

How is ascites managed?

A
  1. Reduce dietary sodium
  2. Aldosterone antagonist - Spironactalone
  3. Drain - needs PT and albumin cover
  4. Prophylactic Abx (prevent SBP)
  5. TIPS - last line, high risk
121
Q

What is paracentesis induced circulatory dysfunction?

A

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.

122
Q

When should you give prophylactic Abx in ascities? Which abx is used?

A

Ascitic albumin concentration <15g/L (found on paracentesis)

Ciprofloxacin PO

123
Q

What is another name for paracentesis?

A

Ascitic tap/drain

124
Q

What is the gold standard diagnostic investigation for SBP?

A

Paracentesis

Neutrophil count >250 cells/ul

125
Q

What percentage of patients with ascites secondary to cirrhosis will develop SBP?

A

10%

126
Q

What is the mortality of SBP?

A

10-20%

127
Q

How does SBP present?

A

• Can be asymptomatic so have a low threshold for ascitic fluid culture
• Fever
• Abdominal pain
• Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
• Ileus
- Hypotension

128
Q

What are the most common organisms that cause SBP?

A

• Escherichia coli
• Klebsiella pnuemoniae
- Gram positive cocci (such as staphylococcus and enterococcus)

129
Q

What is the management of SBP?

A
  • Take an ascitic culture prior to giving antibiotics

- Usually treated with an IV cephalosporin such as cefotaxime

130
Q

What is the pathophysiology of hepatorenal syndrome?

A

Loss of circulating blood volume (portal vessel dilatation, ascites)
Activation of RAAS
Vasoconstriction of renal blood vessels
Deteriorating kidney function

131
Q

What is the prognosis of hepatorenal syndrome?

A

Fatal within a week

Needs liver transplant

132
Q

What is the management of hepatorenal syndrome?

A

Liver transplant

133
Q

What is another name for hepatic encephalopathy?

A

Portosystemic encephalopathy

134
Q

Which toxin causes hepatic encephalopathy?

A

Ammonia

135
Q

Why does ammonia build up in the blood of patients with liver cirrhosis?

A
  • Functional impairment of the liver cells prevents them metabolising the ammonia into harmless waste products.
  • Collateral vessels between the portal and systemic circulation mean that the ammonia bypasses liver altogether and enters the systemic system directly.
136
Q

How does hepatic encephalopathy present?

A

Reduced consciousness
Confusion
Changes to personality, memory and mood

137
Q

What factors can precipitate hepatic encephalopathy?

A 
• Constipation
• Electrolyte disturbance
• Infection
• GI bleed
• High protein diet
- Medications (particularly sedative medications)
138
Q

What is the management of hepatic encephalopathy?

A

• Laxatives (i.e. lactulose) promote the excretion of ammonia. The aim is 2-3 soft motions daily. They may require enemas initially.
• Antibiotics (i.e. rifaximin) reduces the number of intestinal bacteria producing ammonia. Rifaximin is useful as it is poorly absorbed and so stays in the GI tract.
- Nutritional support. They may need nasogastric feeding.

139
Q

Which autoimmune conditions are commonly associated with coeliac disease?

A 
Diabetes type I - all new presentations are tested for coeliac
Thyroid disease
Autoimmune hepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis
140
Q

What are the genetic associations with coeliac disease?

A

• HLA-DQ2 gene (90%)

HLA-DQ8 gene

141
Q

When does coeliac present?

A

Biomodal - infancy & 50-60 years

142
Q

How is the spleen affected by coeliac disease?

A

Hyposplenism

143
Q

How does coeliac disease present?

A

• Failure to thrive in young children
• Diarrhoea
• Fatigue
• Weight loss
• Mouth ulcers
• Anaemia secondary to iron, B12 or folate deficiency
Dermatitis herpetiformis (an itchy blistering skin rash typically on the abdomen)

144
Q

What neurological symptoms can be caused by coeliac disease?

A

• Peripheral neuropathy
• Cerebellar ataxia
Epilepsy

145
Q

What is the gold standard investigation for diagnosing coeliac disease?

A

Jejunal biopsy

146
Q

How is a biopsy taken in suspected coeliac disease?

A

From the jejunum via a Crosby capsule

147
Q

What features are seen on biopsy for coeliac disease?

A

Villous atrophy
Crypt hyperplasia/hypertrophy
Increase in intraepithelial lymphocytes
Lamina propria infiltration with lymphocytes

148
Q

Which three auto-antibodies are associated with coeliac disease? Which is most specific?

A

IgA tissue transglutaminase (TTG) antibodies - specific
Anti-endomysial (anti-EMA)
Deaminated gliadin peptides antibodies (anti-DGPs)

149
Q

Why should you test for IgA levels as well as specific autoantibodies?

A

Some patients have an IgA deficiency. if total IgA is low then the coeliac test will be negative even when they have coeliacs

150
Q

What are the 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)
Dermatitis herpetiformis
151
Q

What is the management of coeliac disease?

A

Life-long gluten free diet

152
Q

Name two dermatological complications of coeliac disease?

A

Dermatitis herpetiformis

Aphthous ulcers

153
Q

Which foods should be avoided in coeliac?

A

Barley
Rye
Oats
Wheat

154
Q

Which foods are okay to eat in coeliac disease?

A

Maise, soya, rice

155
Q

Which vaccination should people with coeliac receive?

A

Pneumococcal (due to hyposplenism)

156
Q

How is the oesophagus anatomically divided?

A

Divided into 3rds: reflects change in musculature from striated → mixed → smooth.

157
Q

Which epithelium lines the oesophagus?

A

• Lined by non-keratinising squamous epithelium.

Z-line: transition from squamous → gastric columnar

158
Q

How can the causes of dysphagia be grouped?

A

Inflammatory
Neurological
Mechanical obstruction

159
Q

Name 4 inflammatory causes of dysphagia.

A

• Tonsillitis, pharyngitis
• Oesophagitis: GORD, candida
• Oral candidiasis
- Aphthous ulcers

160
Q

Name 4 local neurological causes of dysphagia.

A
  • Achalasia
  • Diffuse oesophageal spasm
  • Nutcracker oesophagus
  • Bulbar / pseudobulbar palsy (CVA, MND)
161
Q

Name 2 systemic neurological causes of dysphagia.

A

MG

Systemic sclerosis/CREST syndrome

162
Q

How can the mechanical obstructive causes of dysphagia be grouped?

A

Luminal - FB, food bolus
Mural - stricture, malignancy
Extra-mural - retrosternal goitre, lung ca, mediastinal lymphoma, TAA

163
Q

What is Boerhaave’s syndrome?

A

Oesophageal tear

164
Q

Give some features of an oesophageal tear.

A
  • Odonophagia (painful swallowing)
  • Mediastinitis: tachypnoea, dyspnoea, fever, shock
  • Surgical emphysema
165
Q

What investigations should be done in dysphagia?

A

Upper GI endoscopy

Ba swallow

166
Q

What is indicated by a corkscrew oesophagus on barium swallow?

A

Diffuse oesophageal spasm

167
Q

Why is the incidence of oesophageal cancer increasing?

A

Barret’s oesophagus

168
Q

What is the median age of presentation in oesophageal cancer?

A

50-70 years

169
Q

What are the risk factors for oesophageal cancer?

A 
• EtOH 
• Smoking 
• Achalasia 
• GORD → Barrett’s 
• Plummer-Vinson 
• Fatty diet 
• ↓ vit A+C 
Nitrosamine exposure
170
Q

Which type of cancer is found in the upper and middle thirds of the oesophagus?

A

Squamous cell carcinoma - associated with alcohol, smoking

171
Q

Which type of cancer is found in the lower third of the oesophagus?

A

Adenocarcinoma - associated with Barret’s oesophagus

172
Q

Which type of oesophageal cancer is most common?

A

Adenocarcinoma (65%)

173
Q

How does oesophageal cancer present?

A

Progressive dysphagia (solids –> liquids)
Weight loss
Retrosternal chest pain
Lymphadenopathy

174
Q

How might a malignant mass in the upper third of the oesophagus present?

A

Hoarseness: recurrent laryngeal nerve invasion

Cough –> aspiration pneumonia

175
Q

Where might oesophageal cancer metastasise to?

A

Direct
Lymphatics
Blood

75% of patients have mets at presentation

176
Q

How is oesophageal cancer staged?

A

TNM

CT, US

177
Q

How is oesophageal cancer diagnosed?

A

Upper GI endoscopy + biopsy

178
Q

What is the treatment of oesophageal cancer?

A

MDT
Oesophagectomy (25-30% resectable)
Neo-adjuvant chemo - cisplatin

179
Q

What is the 5 year survival for oesophageal cancer?

A

<5%

180
Q

Name some palliative approaches to oesophageal cancer.

A

Stenting
Radiotherapy
Analgesia
Macmillan nurses & palliative care referral

181
Q

What is achalasia?

A

Degeneration of myenteric plexus (Auerbach’s)
↓ peristalsis
LOS fails to relax

182
Q

What are the two causes of achalasia?

A

1O / idiopathic: commonest

2O: Chagas’ disease (T. cruzii)

183
Q

How does a patient present with achalasia?

A

Dysphagia: liquids –> solids
Regurgitation
Weight loss
Substernal cramps

184
Q

Give a complication of achalasia.

A

SCC of the oesophagus (3-5%)

185
Q

What is seen on barium swallow in achalasia?

A

dilated tapering oesophagus - Bird’s beak

186
Q

What can be seen on CXR in achalasia?

A

widened mediastinum, double RH border

187
Q

How is achalasia managed?

A
  • Medical - CCBs, nitrates
  • Interventions: botox injection, endoscopic balloon dilatation
  • Surgical: Heller’s cardiomyotomy
188
Q

What is a pharyngeal pouch?

A

Outpouching between crico- and thyro-pharyngeal components of the inf. pharyngeal constrictor.
Area of weakness - Killan’s dehiscence

189
Q

What might be seen on examination on someone with a pharyngeal pouch?

A

Bulge on left side of the neck

190
Q

How might someone present with a pharyngeal pouch?

A

Regurgitation, halitosis, gurgling sounds

191
Q

What is the treatment for a pharyngeal pouch?

A

Excision

Endoscopic stapling

192
Q

How does GORD present?

A 
• Heartburn
• Acid regurgitation
• Retrosternal or epigastric pain
• Bloating
• Nocturnal cough
Hoarse voice
193
Q

Which patients should be admitted for an urgent endoscopy?

A

Signs of GI bleed:

  • Melaena
  • Coffee ground vomiting
194
Q

When should patients have a 2WWW for endoscopy?

A
  • Dysphagia (difficulty swallowing) at any age gets a two week wait referral
  • Aged over 55 (this is generally the cut off for urgent versus routine referrals)
  • Weight loss
  • Upper abdominal pain / reflux
  • Treatment resistant dyspepsia
  • Nausea and vomiting
  • Low haemoglobin
  • Raised platelet count

OR if symptoms >4 weeks with treatment

195
Q

What is the gold standard test for diagnosing GORD?

A

24-hr oesophageal pH monitoring

196
Q

What advice should be given to patients with GORD?

A 
• 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
197
Q

What is the surgical treatment of GORD?

A

Laparoscopic fundoplication

198
Q

What is the treatment of endoscopically proven oesophagitis?

A

• full dose proton pump inhibitor (PPI) for 1-2 months
• if response then low dose treatment as required
- if no response then double-dose PPI for 1 month

199
Q

What is the treatment of endoscopically negative reflux disease?

A

• full dose PPI for 1 month
• if response then offer low dose treatment, possibly on an as-required basis, with a limited number of repeat prescriptions
if no response then H2RA or prokinetic for one month

200
Q

What is H.Pylori?

A

gram negative aerobic bacteria

201
Q

How does H.Pylori cause dyspepsia?

A

exposes the epithelial cells underneath to acid

also produces ammonia to neutralise the stomach acid. The ammonia directly damages the epithelial cells

202
Q

Name four associated conditions of H.Pylori.

A 
• peptic ulcer disease 
	○ 95% of duodenal ulcers
	○ 75% of gastric ulcers
• gastric cancer
• B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
- atrophic gastritis
203
Q

Who should be offered H.Pylori testing?

A

Anyone with dyspepsia

204
Q

Which three tests are used for H.Pylori?

A

• Urea breath test using radiolabelled carbon 13
• Stool antigen test
- Rapid urease test can be performed during endoscopy.

205
Q

How long do patients need to be off PPIs before testing for H.Pylori?

A

2 weeks

206
Q

When can you take a urea breath test?

A

off abs 4 weeks

off PPIs 2 weeks

207
Q

How is H.Pylori treated?

A

Triple therapy:

a proton pump inhibitor (e.g. omeprazole) plus 2 antibiotics (e.g. amoxicillin and clarithromycin) for 7 days.

208
Q

What is used to test for eradication?

A

urea breath test

209
Q

What is Barrett’s oesophagus?

A

metaplasia of the lower oesophageal mucosa

Squamous cell –> columnar

210
Q

Which condition is associated with Barrett’s oesophagus?

A

Adenocarcinoma

211
Q

What are the two types of Barrett’s oesophagus?

A

Short <3cm

Long >3cm

212
Q

When should patients with metaplasia receive endoscopic surveillance?

A

every 3-5 years

213
Q

What is the management of dysplasia?

A

• endoscopic mucosal resection

- radiofrequency ablation

214
Q

Laxative abuse can result in which bowel condition?

A

Melanosis coli

FINALS (26 decks)

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