Brainscape's Knowledge GenomeTM

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


See full index

Passmed > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

What is biliary colic?

A

Biliary colic is crampy abdominal pain in the RUQ caused by a gallstone being intermittently stuck in the neck of the bladder/ cystic duct after gallbladder contraction

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

What are the symptoms of biliary colic?

A

RUQ pain
Radiation to right shoulder and scapula
Nausea
Vomiting
Intolerance for fatty foods

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

How is biliary colic diagnosed?

A

Liver function tests will be normal
Bloods will be normal
Ultrasound: shows gallstones in a thin walled gall bladder

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

How does biliary colic often present?

A

Usually after eating a fatty meal: pain may start a few hours after finishing the meal. Patient will have had recurrent episodes of pain in the past

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

How is biliary colic treated?

A

Analgesia, antiemetics, IV fluids
Elective laprascopic cholecystectomy

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

What is the normal common bile duct diameter?

A

Less than 6mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is acute cholecystitis?

A

Cholecystitis is inflammation of the gallbladder usually due to gallstones, however, it can also be caused by an infection, hypo perfusion and as a result of parenteral feeding

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

What are the symptoms of acute cholecystitis?

A

RUQ pain
Pain on movement
Fever
Nausea
Vomiting
Jaundice: If stone is impacted in common bile duct

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

Describe the bloods seen in acute cholecystitis?

A

Raised CRP
Raised WBC
Possibly raised ALP, BR, and GGT

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

How do you treat acute cholecystitis?

A

Nil by mouth
IV fluids
IV antibiotics
Laprascopic cholecystectomy within 1 week of diagnosis

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

What clinical signs can be elicited in acute cholecystitis?

A

Murphy sign: pressing on the RUQ and asking patient to inspire, will cause pain and halting of breathing

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

What are some complications of acute cholecystitis?

A

Perforation
Gallbladder empyema
Gangrenous cholecystitis: necrosis and perforation of the gallbladder wall as a result of ischemia following progressive vascular insufficiency.

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

What will an abdominal ultrasound show in cholecystitis?

A

Thickened gallbladder wall
Pericholecystic fluid
Gallstone in neck of gallbladder
Sludge

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

What is ascending Cholangitis?

A

Infection of the common bile duct usually due to impacted gallstone

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

What is the gold standard investigation and intervention for ascending Cholangitis?

A

ERCP

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

What symptoms are seen in Cholangitis?

A

Chariots triad: jaundice, fever, RUQ pain
Nausea
Vomiting
Mental confusion
Hypotension
Tachycardia

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

What imaging is done for Cholangitis?

A

Ultrasound
CT
MRCP

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

How is Cholangitis treated?

A

ERCP +/- sphincterotomy: to remove stones from common bile duct
Stent insertion: strictures
Percutaneus transhepatic cholecystostomy: for patients who are unsuitable for ERCP or where ERCP has failed. Allows drainage of gallbladder contents to relieve symptoms.

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

What are the most common organisms causing Cholangitis?

A

E.coli
Klebsiella
Enterococcus

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

What is choledocholelithiasis?

A

Gallstones in the common bile duct

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

How can choledocholelithiasis present if there is complete obstruction?

A

Abdominal pain
Jaundice
Itching
Pale stools
Dark urine

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

Causes of obstructive jaundice?

A

Gallstones
Cholangiocarcinoma
Pancreatic head cancer
Pancreatitis causing strictures

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

Why does primary biliary Cholangitis cause high cholesterol levels?

A

Cholesterol is one of the molecules found in bile. When the intrahepatic bile ducts become damaged, the flow of bile is reduced, resulting in back pressure. This results in the build up of cholesterol in the blood.

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

What are the 2 main initial symptoms in primary biliary Cholangitis?

A

Fatigue
Pruritus (itch)

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

What symptoms aside from fatigue and itching, can be seen in primary biliary Cholangitis?

A

Jaundice
Xanthomata
Xanthelasma
Pale stools
Dark urine
Hyperpigmentation
Muscle and joint pain
Steatorrhoea
Peripheral oedema
Weight loss

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

Describe the typical presentation of PBC?

A

Middle aged (40-60) white woman presents with fatigue and itching. Bloods show raised ALP and positive AMA.

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

What is Primary biliary Cholangitis?

A

It is an autoimmune condition which causes chronic inflammation of the intrahepatic bile ducts. This results in destruction and cholestasis of bile. This eventually leads to liver scarring and eventually cirrhosis.

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

How is primary biliary Cholangitis diagnosed?

A

Bloods: raised ALP, cholesterol, IgM
Presence of Antimocrobial antiobodies

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

What percentage of patients with PBC test positive for anti microbial antibodies (AMA)

A

98%

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

What is the first line management for PBC?

A

Urodeoxycholic acid: non toxic hydrophilic bile acid. Protects cholangiocytes and makes bile less harmful to epithelial cells.

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

Aside from ursodeoxycholic acid what other treatment is available for PBC?

A

Colestyramine: for itching, reduces intestinal reabsorbtion of bile acids
Replacement of fat soluble vitamins
Bisphosphonates
Immunosuppression: with steroids
Liver transplant

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

What is PSC?

A

Primary sclerosing Cholangitis. It is the inflammation of both the intrahepatic and extrahepatic bile ducts, resulting in damage and sclerosis. This resulted in multi focal bile duct strictures resulting in the restriction of bile flow. Eventually leading to liver damage and cirrhosis.

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

Which auto immune conditions are associated with PSC?

A

Ulcerative colitis
Crohns
HIV

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

How does PSC present in the early stages?

A

Asymptomatic
Raised ALPs

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

What symptoms are seen in PSC?

A

RUQ pain
Jaundice
Pruritus
Fatigue
Weight loss
Hepatomegaly
Splenomegaly

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

What is the gold standard investigation for PSC?

A

MRCP: allows visualisation of biliary tree

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

What investigations are done for PSC?

A

MRCP
LFTs
P-Anca
Colonoscopy
Ultrasound

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

Describe the typical presentation of PSC?

A

White, middle aged male with existing UC, presents with itching and fatigue

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

How is PSC treated?

A

ERCP: ballon dilation and stunting
Liver transplant
UDCA
Cholestyramine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What lifestyle adjustments can be made to aid PSC treatment?

A
  • Reducing alcohol intake
  • fat soluble vitamin supplements
  • osteoporosis screening
  • calcium supplements, bisphosphonates
  • monitor LFTs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the percentage risk for cholangiocarcinoma in PSC patients?

A

10-20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the survival rate for liver transplant in PSC patients?

A

70% 10 year survival rate

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

What are the complications of PSC?

A

Acute bacterial Cholangitis
Cholangiocarcinoma
Cirrhosis: portal hypertension, oesophageal varies
Osteoporosis

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

What conditions are associated with PBC?

A

Sjögren’s syndrome
Rheumatoid arthritis
Thyroid disease

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

In a patient with PBC, when do you refer them for liver transplantation?

A

If bilirubin is > 100 micromils/ litre

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

What are the 5 types of viral hepatitis?

A

A
B
C
D
E

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

Which viral hepatitis is a DNA virus?

A

B

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

Which viral hepatitis is only possible in those with hepatitis B?

A

D

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

Which viral hepatitis is transmitted via the faecal oral route?

A

A and E

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

Which hepatitis viruses are notifiable diseases?

A

All of them

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

Who qualifies for hepatitis A vaccine?

A
  • travelling
  • men who have sex with men
  • frequent injecting drug users
  • chronic liver disease
  • professions: sewage workers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How is Hepatitis A diagnosed?

A

LFTs: deranged
Viral screen for hepatitis A serology
- Anti- HAV IgM
- Anti- HAV Total
- PCR for Hepatitis A RNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

If Hepatitis A serology shows the following what does it indicate:
- positive anti-HAV IgM
- positive anti-HAV IgG

A

Acute hepatitis infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the different phases of symptoms in hepatitis infection?

A

Prodromal phase: flu like symptoms (3-10 days)
- nausea
- vomiting
- headaches
- muscle pain, malaise, fever, fatigue

Icteric phase: 1- 12 weeks
- jaundice, itching, pale stools, dark urine, helatomegaly, splenomegaly,

Convalescent phase: up to 6 months
- Malaise, anorexia, muscle weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How is Hepatitis A treated?

A

Hepatitis A should resolve on its own within 1-6 months
Supportive treatment: rest, hydration
Antiemetics: metoclopramide
Analgesia: paracetamol, ibuprofen, codeine (in mild liver impairment)
Itching: loose clothing, avoid hot showers, cool environment, chlorphenamine

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

How is hepatitis B transmitted?

A

Blood and bodily fluids

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

How is hepatitis B diagnosed?

A

LFTs
Liver ultrasound
Liver biopsy
Hepatitis B serology
HBV-DNA

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

How do you manage acute hepatitis B?

A

Same as Hepatitis A
Repeat Hepatitis serology after 6 months to check if it’s chronic

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

How is chronic hepatitis B treated?

A

Regular review by liver specialist:
- screen for HCC
- monitor serology
- pegylated interferon Alpha
Tenofovir/ entecavir

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

What type of hepatitis B infection does the following results indicate?
HBsAg: Positive
Anti-HBs: negative
HBeAg: positive
Anti-HBe: negative
Anti-HBc IgM: negative
HBV-DNA: positive

A

Chronic hepatitis B: Active

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

When is HBeAg positive?

A

It is positive in acute and chronic (active) infection

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

What is HBeAg a marker of?

A

Active viral replication and increased transmissibility

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

When are babies given the hepatitis b vaccine? What happens if mother is hepatitis B positive?

A

6 in 1 vaccine at 8,12 and 16 weeks
Hep b positive mother: additional doses at 24hrs, 4 weeks and 12 months

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

Which type of hepatitis is curable?

A

C

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

How is hepatitis c diagnosed?

A

Anti-HCV
Hepatitis C RNA

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

What does positive hepatitis RNA indicate?

A

Current hepatitis C infection

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

How is hepatitis c treated?

A

Supportive treatment
Direct acting antivirals: treatment dependant on genotype

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

What is the aim of treatment in hepatitis c?

A

Sustained viral response: undetectable viral load 6 months after completion of therapy

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

How many genotypes of hepatitis c are there? Which are the most common?

A

11
1,2,3

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

What is co infection and superinfection? (Hepatitis B)

A

Co- infection: infected with both hepatitis B and D at the same time
Superinfection: hepatitis B patient is subsequently infected with Hepatitis D

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

Can hepatitis E become chronic?

A

Very rarely and only in immunocompromised patients/ organ transplant patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is the most common hepatitis in the UK?

A

E

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What group of people have the highest mortality rate with hepatitis E?

A

Pregnant women

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

What is pancreatitis?

A

Inflammation of the pancreas

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

What are some causes of pancreatitis?

A

Idiopathic, steroids, ERCP, gallstones, hyperlipidaemia, alcohol

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

How is pancreatitis diagnosed?

A

Serum lipase/ amylase: 3x upper limit
Characteristic symptoms

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

What imaging is done for pancreatitis?

A

Ultrasound
CT: complications

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

How is pancreatitis treated?

A
  • Aggressive fluid resuscitation
  • IV analgesia
  • nutrional support
  • oxygen
  • antibiotics: sepsis, Cholangitis

Surgical:
- ERCP
- percutaneus/ endoscopic drainage

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

What are the complications of pancreatitis?

A

Pseudocysts
Pancreatic abscess
Pancreatic necrosis

80
Q

What is a pancreatic pseudocyst? How is it treated?

A

A pancreatic pseudocyst is a collection of pancreatic fluid surrounded by granulation tissue. These can often be asymptomatic and if symptomatic can resolve on their own. However, they can also become infected and would therefore need drainage. Treatment is cystogastroscopy (endoscopic drainage of cysts)

81
Q

What are complications of pancreatic pseudocysts?

A

Bowel obstruction
Vessel obstruction
Rupture
Infection

82
Q

Describe the process of pancreatic necrosis?

A

Extra ducal release of pancreatic enzymes causing auto digestion as well as hypovolemia (SIRS) resulting in poor perfusion and tissue death. This necrotic tissue can become infective and spread to other organs in the body. Treatment is required once complications or infection have developed. Treatment involves debridement and drainage.

83
Q

What additional symptoms are seen in chronic pancreatitis?

A
  • pain worse after eating
  • steatorrhoea
  • diabetes Mellitus
  • Weight loss
84
Q

In chronic pancreatitis, what can be seen on an x ray?

A

Multiple small calcification foci

85
Q

Which medications can cause pancreatitis?

A

Azathioprine
Mesalazine
Furosemide
Sodium valproate

86
Q

What is the preferred investigation for chronic pancreatitis?

A

CT: 85% specificity

87
Q

How is chronic pancreatitis treated?

A

Lifestyle:
- quit smoking
- reduce alcohol intake
- high calorie, high protein diet

Medical:
- pancreatic enzyme supplementation (croon)
- vitamin supplementation
- analgesia
- insulin regimens
- ERCP: strictures, biliary obstruction
- pancreatic resection

88
Q

Why do cholesterol levels increase in cholestasis?

A

Bile is the normal excretory pathway for cholesterol. If there is reduced flow of bile, cholesterol degradation and secretion is impaired. As a result cholesterol levels build up in the blood.

89
Q

Explain the pathogenesis in appendicitis?

A

Obstruction results in increased luminal pressure. This compromises lymphatic and venous drainage. This results in hypoxia and tissue ischaemia. Obstruction also creates an environment that promotes bacterial growth allowing invasion of bacteria into the appendix. This results in an inflammatory response. This can lead to necrosis and ultimately perforation.

90
Q

What is the proposed function of the appendix?

A

Lymphatic drainage
Production and maintenance of good bacteria

91
Q

What symptoms are seen in acute appendicitis?

A

Umbilical pain moving to RIF
Nausea
Vomiting
Anorexia: loss of appetite
Pain worse on coughing

92
Q

What are the possible causes of appendicitis?

A

Faecoliths
Lymphoid hyperplasia
Foreign body
Malignancy
Direct bacterial invasion

93
Q

What are some differentials for appendicitis?

A

Ovarian cyst
Ectopic pregnancy
Meckels diverticulitis
Testicular torsion
UTI
Pelvic inflammatory disease
Crohns

94
Q

What investigations are done for suspected appendicitis?

A

FBC (neutrophils)
CRP
Urinalysis: HCG
Ultrasound: gynaecological pathology

95
Q

How is uncomplicated appendicitis treated?

A

Appendicectomy: ideally laparoscopic
IV fluids
IV antibiotics

96
Q

What is an appendix mass?

A

This is when the surrounding omentum sticks to the inflamed appendix, forming a mass in the RIF. Initially managed with analgesia and antibiotics. Once resolved an appendicectomy can be performed. Ultrasound and CT

97
Q

If patient presents clinically with appendicitis but investigations are negative, what can be done?

A

Observation: monitor patient and see if there is any improvement, give antibiotics and fluids.
Diagnostic laparoscopy

98
Q

What are some complications of appendicitis?

A

Appendix mass
Abscess formation
Phlegmon

99
Q

What are the 2 types of IBD?

A

Crohns
Ulcerative colitis

100
Q

What symptoms are seen in Crohns?

A

Chronic diarrhoea
Weight loss
Fatigue
Nausea
Vomiting
Abdominal pain: typically right iliac fossa
Mouth ulcers
Perinatal disease: itch, pain, fissures

101
Q

What extraintestinal symptoms can be seen in Crohns?

A

Uveitis: pain on eye movement, photophobia, blurry vision
Erythema nodosum
Pyoderma gangrenosum
Gallstones
Renal stones
Arthritis

102
Q

Explain how Crohns causes fistula formation? What is the most common?

A

Crohns causes chronic inflammation of most frequently the intestine. The inflammation is transmural and affects the whole intestinal wall. This results in tracts forming between the intestinal lumen/ anal canal and nearby structures. This allows the movement of bacteria, air and faeces to enter surrounding structures causing infection resulting in abscess.
The most common being enterovesical (UTI) and perianal (abscess)

103
Q

What signs can be seen on examination in Crohns?

A
  • tenderness in RIF or generalised
  • erythema nodosum
  • absent bowel sounds
    Clubbing
    Pallor
    Red eye
    Perinatal tenderness, reddened skin, abscess
104
Q

What investigations should be done in suspected Crohns ?

A

FBC
CRP
ESR
LFTs
Iron profile/ haematinics
Anti-TTG
Stool sample: culture and fecal cal protection
Colonoscopy + biopsy
MRI/ CT

105
Q

What will colonoscopy show in Crohns?

A

Skip lesions
Cobble stoning
Ulcers

106
Q

What will CT show in Crohn’s disease?

A

Fistulas
Abscesses
Strictures
Bowel wall thickness

107
Q

How is Crohns remission induced?

A

First line: corticosteroids: IV hydrocortisone, prednisone
- If ileocaecal disease/ corticosteroid not tolerated and contraindicated offer budesonide
Second line: single exarcerbation in 12 months/ first presentation and unable to tolerate glucocorticoids offer an aminosalicylate (mesalazine/ sulfasalazine)
Third line: If patient has had 2 or more exarcerbation within the last 12 months/ glucocorticoid cannot be tapered add on a thiopurine (azathioprine) or methotrexate
Fourth line: Biologics (infliximab) severe Crohn’s disease

108
Q

What must be assessed before starting a thiopurine?

A

TPMT: thiopurine methyltransferase activity

109
Q

What is the first line and second line medication for remission maintenance in Crohns?

A

Azathioprine
Methotrexate

110
Q

What surgical options are available for Crohns?

A

Resection of distal ileum
Segmental bowel resections
ERCP stricture ballooning
Abscess drainage
Fistula removal

111
Q

What should patients with Crohns be advised to do first and foremost?

A

QUIT SMOKING

112
Q

What type of drug is infliximab?

A

Anti- tumour necrosis factor alpha

113
Q

When should budenoside be offered instead of a corticosteroid for Crohns?

A

If it’s the patients first presentation or they have had a single exarcerbation in the last 12 months
And
Unable to tolerate/ contraindicated to glucocorticosteroids?

114
Q

What should be first line treatment in children and adolescents with Crohns exarcerbation? Why?

A

Enteral nutrition. This is due to concerns about growth or side effects

115
Q

How is a mild to moderate exarcerbation of ulcerative colitis treated?

A

First line: topical aminosalicylate (mesalazine), if remission not induced within 4 weeks change to oral
Second line: If remission still not induced add oral or topical corticosteroid

116
Q

How is severe a exarcerbation of ulcerative colitis treated?

A

First line: IV corticosteroid (hydrocortisone)
If steroid is not tolerated or contraindicated give IV ciclosporin
Second line: If within 72 hours no improvement add IV ciclosporin
Third line: Surgery-

117
Q

How is remission maintained in mild, moderate and severe ulcerative colitis?

A

Mild to moderate:
First line: Aminosalicyclate (topical) or both oral and topical aminosalicylate
Severe: oral azathioprine (methotrexate)

118
Q

How does ulcerative colitis show on colonoscopy?

A

Uniformed ulceration of the mucosa
Granulation
Pseudopolyps

119
Q

How does ulcerative colitis present on biopsy?

A

Crypt abscesses
Crypt distortion
Inflammation extending to submucosa only

120
Q

What are the complications of ulcerative colitis?

A

Toxic mega colon
Perforation
Colorectal cancer

121
Q

How often should patients with ulcerative colitis have a colonoscopy?

A

Everyone should have one 10 years after the first onset of symptoms. After that it is dependant on the extent of disease

122
Q

What symptoms are seen in coeliac disease?

A

Abdominal pain
Abdominal cramping
Weight loss
Fatigue
Inability to thrive
Bloating
Diarrhoea steatorrhoea
Nausea
Vomiting

123
Q

What investigations are done for suspected coeliac?

A

Anti-ttg
Anti-EMA
Serum IgA
Duodenal biopsy

124
Q

Why is serum IgA needed in coeliac investigations?

A

A low serum IgA can give a false negative for anti-ttG antibodies

125
Q

What does a biopsy show in coeliac disease?

A

Crypt hyperplasia
Villus atrophy

126
Q

When should anti-EMA be done for coeliac?

A

If the anti-tTG antibodies come back equivocal or slightly raised

127
Q

If serum IgA is low what test should be done for coeliac disease?

A

IgG anti-tTg, anti-SMA or anti-DGP

128
Q

What is the mainstay of treatment for coeliac disease?

A

Gluten free diet

129
Q

What monitoring should be done for coeliac?

A

Children: BMI, growth and nutritional status
DEXA scan: osteoporosis
Annually:
- coeliac serology to check adherence
- thyroid function tests
- micronutrients
- type 1 diabetes

130
Q

Which cancers are coeliac patients at an increased risk of?

A

Enteropathy-associated t-cell lymphoma (EATL): rare, aggressive non Hodgkin lymphoma, associated with refractory coeliac disease.

Small bowel adenocarcinoma

131
Q

Which 2 genes are associated with coeliac disease?

A

HLA-DQ2
HLA-DQ8

132
Q

In how many cases is coeliac often asymptomatic?

A

1/3rd

133
Q

What extraintestinal symptoms are seen in coeliac disease?

A
  • osteoporosis
  • subfertility and miscarriages
  • anaemia
  • dermatitis herpetiformis
  • angular stomatitis
134
Q

What is the mechanism behind osteoporosis in coeliac disease?

A

Low calcium and vitamin D absorption resulting in compensatory secondary hyperparathyroidism

135
Q

What is IBS?

A

Irritable bowel syndrome
It is a functional disorder due to a disruption in the brain gut connection resulting in abnormal gastrointestinal motility and visceral hypersensitivity

136
Q

When should a diagnosis of IBS be considered?

A

If patient has had 6 months of the one of the following:
- abdominal pain
- Abdominal bloating
- altered bowel habits

137
Q

When can a positive diagnosis of IBS be made in primary care?

A

If patient has abdominal pain/ discomfort for 6 months that is either relieved on defecation or is associated with altered bowel frequency or stool form, and 2 of the following:
- stool urgency, straining, incomplete evacuation
- mucus
- abdominal bloating, hardness, distension
- worse on eating

138
Q

What is the ROME IV criteria for IBS diagnosis in secondary care?

A

Patient must have recurrent abdominal pain at least once a week I. The last 3 months, with symptom onset being 6 months ago, associated with 2 or more of the following:
- pain related to defecation
- change in frequency of stool
- change in consistency of stool

139
Q

What are some extra intestinal symptoms that can be seen in IBS?

A

Lethargy
Nausea
Back pain
Headache

140
Q

What are some common triggers for IBS?

A

Caffeine
Alcohol
Diet
Stress
Anxiety
Depression
Medications (opioids

141
Q

What investigations are done for IBS?

A

IBS is a diagnosis by exclusion.
FBC: anaemia
CRP
ESR
Coeliac serology
Faecal cal protection
Ca125
Measure patient BMI and diet

142
Q

How is IBS managed initially?

A

Lifestyle advice:
- Exercise
- balanced diet
- reduce caffeine
- reduce stress
- reduce alcohol
- regulate fibre intake
- drink plenty of fluid

If unsuccessful refer patient to dietician for specialised dietary advice : Low fodmap

143
Q

What is first line pharmacological treatment for IBS symptoms? When should efficacy be reviewed?

A

Constipation: bulk forming laxatives
Diarrhoea: loperamide
Pain: antispasmodic agents (peppermint oil, mebeverine hydrocjloride)
Efficacy should be reviewed after 3 months

144
Q

If IBS symptom of constipation persists after 12 months despite maximal dose of laxatives, what medication should be given and when should the patient be reviewed?

A

Linaclotide, review after 12 weeks

145
Q

What second line treatment is available for IBS?

A

TCA: amitriptyline
SSRI: citaprolam, fluoxetine
CBT: if refractory

146
Q

What are the 4 classifications of IBS? What are the classifications based on?

A

IBS- C
IBS- D
IBS- M
IBS- U
Based on Bristol stool chart

147
Q

What are the red flag symptoms in suspected GORD that should be referred for 2 week wait OGD?

A

Dysphagia
Persistent symptoms despite treatment
Age > 55
Weight loss
Excessive nausea and vomiting
GI bleeding ( malaena/ coffee ground)
Symptoms > 4 weeks

148
Q

How is how should uninvestigated GORD symptoms be treated?

A

Lifestyle changes
Drugs:
- 4 week course of PPI
- If symptoms return offer low dose of PPI for 1-2months
- If no response offer H2 receptor antagonist

149
Q

How should confirmed GORD be treated?

A
  • 4-8 week course of full dose PPI
  • offer h2RA if PPI inadequate
  • 8 week course if severe oesophagitis ( if fails then high dose of PPI)
  • if symptoms recur then offer PPI at low dose long- term/ as needed
150
Q

What can h.pylori infection cause?

A

Peptic ulcers
Gastritis
Increased risk of gastric cancer
Functional dyspepsia

151
Q

What tests are done for h.pylori?

A

Stool antigen test
Urea breath test
Rapid urease tests.pylori serum antibody test
Gastric biopsy culture

152
Q

Which tests for h.pylori are first line?

A

Stool antigen
Urea breath test

153
Q

How is h.pylori managed first line?

A

Triple therapy, 7 day course of:
NPA: PPI + amoxicillin + clarithromycin/ metronidazole
PA: PPI + clarithromycin + metronidazole

154
Q

How long after initial therapy should you retest for h.pylori?

A

If poor compliance to first line therapy retest for h.pylori 4-8 weeks after

155
Q

How long must a patient with suspected coeliac be eating gluten for before serology testing?

A

6 weeks

156
Q

What are the risk factors for Barrett’s oesophagus?

A

Smoking
GORD
Central obesity
Male

157
Q

How is Barrett’s oesophagus treated?

A

High dose PPI
Endoscopic surveillance
If dysplasia is found: endoscopic ablation or endoscopic mucosal resection

158
Q

Which cancer does Barrett’s oesophagus increase the risk for?

A

Oesophageal adenocarcinoma

159
Q

What is the most common cause of peptic ulcers?

A

H. Pylori

160
Q

What are the symptoms of peptic ulcers?

A

Nausea
Epigastric pain (radiate to back)
Haematemesis
Dyspepsia
Pain relieved or worsened by eating

161
Q

Which type of peptic ulcer is worse on eating?

A

Gastric ulcer

162
Q

What investigations are done for suspected peptic ulcer?

A

FBC: microcytic anaemia
Urea breath test
Stool antigen test
Endoscopy: if red flag symptoms

163
Q

What are the complications for peptic ulcers?

A

Perforation
Bleeding

164
Q

What are some causes of an upper GI bleed?

A

Mallory Weiss tear
Oesophagitis
Oesophageal varies
Peptic ulcers
Gastric cancer

165
Q

What are the symptoms of an upper GI bleed?

A

Haematemesis
Malaena

166
Q

How should an upper GI bleed be treated?

A

Risk assessment: blatchford
Resuscitation: oxygen, fluids
Blood transfusion: do not offer if not actively bleeding/ haemodynamically stable
Platelet transfusion: if platelet count below 50L
Fresh frozen plasma: If INF 1.5x normal
Prothrombin complex concentrate: offer to patients on warfarin and actively bleeding
Endoscopy within 24 hours: treatment based on cause

167
Q

How should a oesophageal variceal bleed be treated?

A

Terlipressin
Prophylactic antibiotic
Band ligation
Transhugukar I translated portosystemic shunt (TIPS): if not controlled by band ligation

168
Q

How do you treat a non variceal upper GI bleed?

A

PPI only after endoscopy
Mechanical clips
Thermal coagulation with adrenaline

169
Q

Why is there an increase in urea in an upper GI bleed?

A

Acid and enzymes break down blood from bleed. Breakdown produces proteins which are absorbed in the GI tract, there is adequate time due to it being an upper GI bleed. Protein is then metabolised in the liver producing urea.

170
Q

What are the 3 stages to alcoholic liver disease?

A

Fatty liver
Hepatitis
Cirrhosis

171
Q

What tests are done for suspected alcoholic liver disease?

A

FBC
LFTs
U&Es
Haematinics
Viral hepatitis serology
Ultrasound
AMA
Liver biopsy
Endoscopy

172
Q

What clinical signs can be seen in alcoholic liver disease?

A

Hands:
Palmar erythema
Dupuytrures contracture
Clubbing

Chest:
Spider naevi
Gynecomastia
Ascites
Hepatomegaly
Splenomegaly
Loss of hair
Reduced libido

173
Q

How is alcoholic liver disease managed?

A

Alcohol abstinence
Weight loss
Nutrition: high protein diet
Vaccinations
Corticosteroids
Treatment for oesophageal varices and ascites

174
Q

How is ascites treated?

A

Low sodium diet
Reduce fluid intake if sodium is less than 125
Spironolactone
Prophylactic antibiotics (citaprolam)
Drainage

175
Q

What is the time frame for alcohol withdrawal symptoms?

A

6-12 hrs: sweating, tremor, headache, nausea
12-24hrs: hallucinations
24-48: seizures (tonic-clonic)
48-72hrs: delirium tremens

176
Q

What is delirium tremens?

A

Medical emergency due to alcohol withdrawal. GABA under-functions and glutamate over-functions due to sudden alcohol withdrawal. Can lead to wernicke-korsakoff syndrome

177
Q

How is alcohol withdrawal managed?

A

benzodiazepines (diazepam/ chlordiazepoxide)
Carbamazepine as alternative
Pabrinex (IV or IM)
Long term thiamine

178
Q

What increases risk of wernicke- Korsakoff’s syndrome?

A

Malnourished
Risk of malnourishment
Existing liver disease

179
Q

What is encephalopathy?

A

Disturbance to brain function due to infection/ injury

180
Q

In patients with delirium tremens what medication should they be given?

A

Lorazepam first line
Haloperidol/ IV lorazepam second line

181
Q

What are the side effects for metoclopramide?

A

Diarrhoea
Dystonia: involuntary muscle contraction
Dyskinesia: involuntary body movement
Avoid in bowel obstruction

182
Q

What are the risk factors for clostridium difficile?

A

Antibiotics
PPI

183
Q

What symptoms are seen in clostridium difficile infection?

A

Diarrhoea
Abdominal pain
Toxic mega colon
Fever

184
Q

How is c.difficile diagnosed?

A

Stool culture to detect the c.difficile toxin

185
Q

How is c.difficile treated?

A

First line: oral vancomycin for 10 days
Second line: oral fidaxomicin
Third line: oral vancomycin + IV metronidazole

186
Q

How is oesophageal variceal haemorrhage prevented?

A

Propranolol
Endoscopical variceal band ligation + PPI (to prevent ulcers)
TIPS

187
Q

If a patient presents with ongoing symptoms within 12 weeks of c.diff treatment what antibiotic should they be given?

A

Oral fidaxomicin

188
Q

Which gene is responsible for haemochromatosis?

A

HFE gene : chromosome 6

189
Q

What auto antibodies are associated with autoimmune hepatitis?

A

ANA
Anti-SMA
P-ANCA
LC-1
LKM-1

190
Q

How is autoimmune hepatitis treated?

A

Moderate to severe: immunosuppressive with prednisolone or azathioprine
Vaccinations against hep b and c
Yearly dexa scan
Calcium and vitamin d supplements

191
Q

What are possible causes of a serum albumin gradient (SAAG) greater than 11g/L?

A

Portal hypertension causes:
Cirrhosis
Alcoholic liver disease
Liver metastasis
Right heart failure

192
Q

What are the adverse effects of PPIs?

A

Hypomagnesia
Hyponatraemia
Osteoporosis
Increased risk of c.difficile infection

193
Q

What blood results are indicative of haemochromatosis?

A

High transferritin
Raised or normal ferritin
Low total iron binding capacity

194
Q

What are some symptoms of haemochromatosis?

A

Bronze skin
Diabetes mellitus
Hepatomegaly
Cirrhosis
Heart failure
Arthritis
Fatigue
Erectile dysfunction

195
Q

How is autoimmune hepatitis diagnosed?

A

Diagnosis is via liver biopsy showing hepatocyte swelling, interface hepatitis, plasma cell infiltration and necrosis

196
Q

In which 2 locations are coeliac biopsy’s done? Which is more common?

A

Jejunum and duodenum
Duodenum is more common

197
Q

What are the symptoms seen in autoimmune hepatitis?

A

asymptomatic
Jaundice
Fatigue
Cirrhosis
Anorexia
Weight loss
Ammenorrhoea
Pruritus
Pyrexia

Passmed (5 decks)

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