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Alice's finals cards > GI > Flashcards

GI Flashcards

1
Q

What are the 3 steps of alcoholic liver disease?

A

Alcohol related fatty liver
alcoholic hepatitis
Cirrhosis

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2
Q

What is the recommended alcohol consumption in a week?

A

14 units a week spread over 3 days. No more than 5 units in a day

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3
Q

What is the screening tool for harmful alcohol use and what are the questions?

A

CAGE questionaire

C- have you ever thought about cutting down?
A- do you get annoyed when other people comment on your drinking?
G- do you ever feel guilty about your drinking?
E- eye-opener. Ever drink in the morning to help with your hangover/ nerves

AUDIT questionnaire is a better way of screening but is longer

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4
Q

What do blood tests show in alcohol abuse?

A

FBC- raised MCV
LFTs- ALT and AST raised. Gamma GT is escpecially high. Low albumin due to reduced synthetic function of the liver

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5
Q

What can be seen on ultrasound of a fatty liver?

A

Increased echogenicity

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6
Q

Which scan is used to assess cirrhosis?

A

Fibroscan

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7
Q

Which test is used to confirm alcohol related liver changes?

A

Biopsy

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8
Q

What is the timeline of symptoms in alcohol withdrawal?

A

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

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9
Q

What are the symptoms of delirium tremens?

A

Acute confusion
Severe agitation
Delusions and hallucinations
Tremor
Tachycardia
Hyperthermia

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10
Q

Which tool can be used to score patients withdrawing from alcohol?

A

CIWA-Ar

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11
Q

How is alcohol withdrawal managed?

A

Chlordiazepoxide
Pabrinex

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12
Q

What causes korsakoffs syndrome?

A

Thiamine deficiency

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13
Q

What is the triad of symptoms found in wernicke’s encephalopathy

A

Confusion
Oculomotor disturbances
Ataxia

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14
Q

What are the features of korsakoff’s syndrome?

A

Memory impairment
Behavioural changes

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15
Q

What are the 4 most common causes of liver cirrhosis?

A

Alcoholic liver disease
Non-alcoholic liver disease
Hepatitis B
Hepatitis C

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16
Q

What is seen on bloods in someone who has liver cirrhosis?

A

LFTs are often normal but in decompensated cirrhosis, all LFTs are deranged

Albumin and PT are useful markers of synthetic function. Will be lower in worse disease

Hyponatraemia indicates fluid retention in severe disease

Alpha-fetoprotein is a marker for HCC and should be checked every 6 months

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17
Q

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

A

ELF blood test (enhanced liver fibrosis)

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18
Q

What is seen on ultrasound of a cirrhotic liver?

A

Nodularity of the surface
Corkscrew appearance of the arteries

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19
Q

How is cirrhosis scored?

A

using the child-pugh socre. The minimum score is 5 and the max is 15

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20
Q

Where do varices usually occur?

A

Gastro-oesophageal junction
Ileocaecal junction
Rectum
anterior abdominal wall

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21
Q

How can varices be managed?

A

propanolol reduces portal hypertension
Elastic band ligation
Injection of sclerosant
Transjugular intra-hepatic portosystemic shunt

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22
Q

how can bleeding oesophageal varices be managed?

A

Vasopressin analogues
Correct coagulopathy with vitamin K and fresh frozen plasma
Urgent endoscopy

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23
Q

How does spontaneous bacterial peritonitis present?

A

asymptomatic
Fever
Abdominal pain
derranged bloods
Ileus
Hypotension

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24
Q

What is the management of Spontaneous bacterial peritonitis?

A

IV cephalosporins such as cefotaxime

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25
Q

What are the 4 stages of non-alcoholic fatty liver disease?

A
  1. NAFLD
  2. Non-alcoholic steatohepatitis
  3. Fibrosis
  4. Cirrhosis
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26
Q

What is the test which can confirm NAFLD?

A

Ultrasound

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27
Q

What are the first and second line recommended investigations for assessing fibrosis?

A

Enhanced liver fibrosis blood test (ELF test)

NAFLD fibrosis score

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28
Q

What is the management of NAFLD?

A

Weight loss
Exercise
Stop smoking
Control of diabetes
Avoid alcohol

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29
Q

What are the symptoms of hepatitis?

A

Abdominal pain
Fatigue
Itching
Muscle and joint aches
Nausea and vomiting
Jaundice
Fever (if viral)

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30
Q

What do the LFTs look like in hepatitis?

A

Raised transaminases (AST/ALT) with proportionally less of a raise in ALP

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31
Q

What type of virus is hepatitis A?

A

RNA

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32
Q

How is hepatitis A transmitted?

A

Faeco-oral route

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33
Q

What type of virus is hepatitis B?

A

DNA virus

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34
Q

What does a high number or surface antigen (HBsAg) imply?

A

Active infection

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35
Q

What does a high level of E-antigen (HBeAg) suggest?

A

Marker of viral replication and implies high infectivity

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36
Q

What do Anti-HBc suggest

A

Implies past or current infection

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37
Q

What does Anti-HBs suggest

A

implies immunity (exposure or immunisation)

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38
Q

What type of virus is Hepatitis C?

A

RNA

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39
Q

How is hepatitis C screened for?

A

Hep C antibody is the screening test
Hep C RNA testing is used to confirm the diagnosis of hep C

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40
Q

What kind of virus is hepatitis D?

A

RNA

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41
Q

What type of virus is hepatitis E?

A

RNA

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42
Q

Which hepatitis can only survive in co-infection with hepatitististis B?

A

D

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43
Q

Which age group does type 1 autoimmune hepatitis affect?

A

Adults

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44
Q

Which age group does type 2 autoimmune hepatitis affect?

A

Children (el nino)

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45
Q

What is the treatment of autoimmune hepatitis?

A

Prednisolone

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46
Q

What is haemochromatosis?

A

An iron storage disorder which results in excessive total body iron and deposition of iron in tissues

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47
Q

What inheritance pattern is haemochromatosis?

A

Autosomal recessive

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48
Q

When does haemochromatosis present?

A

Typically after the age of 40 when the iron load becomes symptomatic. Presents later in females due to menstruation

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49
Q

What are the symptoms of haemochromatosis?

A

Memory and mood disturbance
Hair loss
Chronic tiredness
Skin pigmentation (bronze)
Erectile dysfunction/ ammenorrhea
Joint pain

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50
Q

How is haemochromatosis diagnosed?

A

Serum ferritin. This is an acute phase reactant so a serum transferritin should also be performed to see if there is iron overload (high) or infection/ NAFLD (low)

Liver biopsy with Perl’s stain

CT abdo

MRI

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51
Q

What are the complications of haematochromatosis?

A

Cardiomyopathy (iron deposits in the heart)
HCC/liver cirrhosis
Hypothyroidism
Arthropathy

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52
Q

What is the management of haemochromatosis?

A

Venesection
Monitoring serum ferritin
Desferrioxamine may be used second line
Avoid alcohol
Genetic counselling

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53
Q

What is wilson’s disease?

A

Excessive accumulation of copper in the body

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54
Q

What is the genetic inheritance of wilson’s disease?

A

Autosomal recessive

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55
Q

What is the presentation of wilsons disease?

A

Dysarthria, dystonia, parkinsonism - basal ganglia degenration

Psychosis or depression

Kayser-fleischer rings in the cornea

Liver cirrhosis

Haemolytic anaemia

Osteopenia

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56
Q

How is Wilson’s disease diagnosed?

A

Serum caeruloplasmin (low is suggestive of Wilson’s)

Liver biopsy is the gold standard

24 hour urine copper assay

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57
Q

What is the management of Wilson’s disease?

A

Penicillamine

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58
Q

What is the pathophysiology of alpha-1-antitrypsin deficiency?

A

Elastase is an enzyme which is secreted by neutrophils and this enzyme digests connective tissues. Alpha-1-antitrypsin is mainly produced in the liver and it inhibits the neutrophil elastase enzyme. Without this there is liver cirrhosis, bronchiectasis and emphysema

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59
Q

What are the features of alpha-1-antitrypsin deficiency?

A

Liver cirrhosis after 50 years old
Bronchiectasis and emphysema after 30 years old

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60
Q

How is alpha-1-antitrypsin deficiency diagnosed?

A

Low serum alpha-1-antitrypsin

Liver biopsy shows cirrhosis and acid-schiff-positive staining globules

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61
Q

What is the management of alpha-1-antitrypsin deficiency?

A

Stop smoking
Symptomatic management
Organ transplant

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62
Q

What is primary biliary cirrhosis?

A

Immune system attacks the small bile ducts within the liver. Causes cholestasis which leads to increased back pressure, fibrosis, cirrhosis and liver failure

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63
Q

What is the presentation of primary biliary cirrhosis?

A

Fatigue
Pruritis
GI pain
Jaundice
Pale stools
Xanthoma

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64
Q

How is primary biliary cirrhosis diagnosed?

A

ALP is raised

Anti-mitochrondrial antibodies raised

Liver biopsy

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65
Q

What is the management of primary biliary cirrhosis?

A

Urseodeoxycholic acid (reduces GI uptake of cholesterol)

Colestyramine prevents bile acid sequestration in the gut

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66
Q

What is primary sclerosing cholangitis?

A

Intrahepatic or extrahepatic ducts become strictured or fibrotic which leads to chronic bile obstruction

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67
Q

Which other disease is primary sclerosing cholangitis strongly associated with?

A

Ulcerative colitis

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68
Q

What is the presentation of primary sclerosing cholangitis?

A

Jaundice
Chronic RUQ pain
Pruritis
Fatigue
Hepatomegaly

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69
Q

How is primary sclerosing cholangitis diagnosed?

A

Gold standard is an MRCP

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70
Q

What is the management of primary sclerosing cholangitis?

A

Liver transplant (curative)
Colestyramine
ERCP

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71
Q

What are the main risk factors for HCC?

A

Viral hepatitis (B and C)
Alcohol
NAFLD

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72
Q

Which cancer is primary sclerosing cholangitis related to?

A

Cholangiocarcinoma

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73
Q

What is the tumour marker for HCC?

A

Alpha-fetoprotein

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74
Q

What is the tumour marker for cholangiocarcinoma?

A

CA19-9

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75
Q

What is the lining of the oesophagus?

A

Squamous epithelial lining

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76
Q

What is the lining of the stomach?

A

Columnar epithelia lining

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77
Q

What is the presentation of GORD?

A

Heartburn
Acid regurg
Retrosternal or epigastric pain
Bloating
Nocturnal cough
Hoarse voice

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78
Q

What are the red flag symptoms for 2 week wait referral?

A

Dysphagia
>55
Weight loss
N+V
Low haemoglobin
raised Platelet count

79
Q

What is the management of GORD?

A

Lifestyle advice (smaller, regular meals, weight loss, avoid acidic and spicy food)

Gaviscon and Rennie

PPI- omeprazole, lansoprazole

Ranitidine

Laparoscopic fundoplication

80
Q

Why does H.pylori cause dyspepsia?

A

It breaks into the gastric mucosa to avoid the stomach acid which damages the lining

It produces ammonia to neutralise the stomach acid

81
Q

How is H.pylori tested for?

A

Need to have 2 weeks without PPI for accurate results

Urea breath test

Stool antigen test

Rapid urease test

82
Q

How is H.pylori eradicated?

A

Triple therapy: PPI + 2 antibiotics for 7 days (usually clarithromycin and amoxicillin)

83
Q

What is Barret’s oesophagus?

A

When constant acid reflux metaplasia from squamous to columnar epithelium. It is managed with PPIs and monitoring

84
Q

What is the presentation of peptic ulcers?

A

Epigastric discomfort
N+V
Dyspepsia
Bleeding causing haematemesis
Iron deficiency anaemia

85
Q

How does eating effect the pain of a gastric ulcer vs a duodenal ulcer?

A

Eating worsens the pain of gastric ulcers and improves the pain of duodenal ulcers

86
Q

What is the management of peptic ulcers?

A

High dose PPI

87
Q

How are peptic ulcers diagnosed?

A

Endoscopy. During endoscopy a rapid urease test (CLO) would be performed to check for H.pylori

88
Q

What are the common causes of upper GI bleeding?

A

Oesophageal varices
Mallory-weiss tear
Ulcers of the stomach or duodenum
Cancers of the stomach or duodenum

89
Q

What is the presentation of an upper GI Bleed

A

Haematemesis
Coffee-ground vomit
Malaena
Haemodynamic instability

90
Q

What is the scoring system used in suspected upper GI bleed?

A

Glasgow-blatchford score. A score >0 indicates a bleed

91
Q

Why does serum urea increase in GI bleed?

A

Urea is a breakdown product when blood is digested within the GI tract

92
Q

What is the rockall score?

A

Used for patients who have had an endoscopy to calculate their risk of rebleeding

93
Q

What is the management of upper GI bleed?

A

ABATED
A-ABCDE
B-Bloods
A-Access
T-Transfuse. crossmatch 2 units
E-Endoscopy
D-Drugs (stop anticoag)

94
Q

What should be given if oesophageal varices are suspected as a cause of upper GI bleed?

A

Terlipressin
Prophylactic broad spectrum antibiotics

95
Q

What are the features of Crohn’s disease?

A

NESTS
N-No blood or mucus
E- Entire GI tract
S- Skip lesions
T- Terminal ileum is most affected. Transmural
S- Smoking is a risk factor

96
Q

What are the features of UC?

A

CLOSEUP

C-continuous inflammation
L- limited to colon and rectum
O- only superficial mucosa
S- Smoking is protective
E- Excrete blood and mucus
U- Use aminosalicylates
P- primary sclerosing cholangitis

97
Q

How do you test for IBD?

A

CRP indicated inflammation and active disease

Faecal calprotectin is a sensitive and specific screening test

98
Q

What is the management of Crohn’s?

A

Induce remission through steroids

Add immunosupression if doesn’t work (azathiopurine)

Maintain remission through azathiopurine or mercaptopurine

99
Q

What is the management of UC?

A

Induce remission:
1st amiosalicylate such as mesalazine
2nd steroids

Maintain remission:
Mesalazine

Surgery: removing colon and rectum

100
Q

What are the symptoms of IBS?

A

Diarrhoea
Constipation
Fluctuating bowel habit
Abdominal pain
Bloating
Worse by eating
Improved by opening bowels

101
Q

How should IBS be investigated?

A

Normal bloods
Do faecal calprotein to exclude IBD
Do anti-TTG antibodies to exclude coeliac

102
Q

How is IBS managed?

A

Low FODMAP diet
CBT
Loperamide for diarrhoea
Laxatives for constipation
Antispasmodics for cramps (buscopan)

103
Q

Which 2 antibodies are associated with coeliacs disease?

A

anti-tissue transglutaminase (anti-TTG) and anti-endomysial (anti-EMA)

104
Q

What is seen on histology of the bowel mucosa in coeliac’s?

A

Villous atrophy
Crypt hypertrophy

105
Q

Which autoimmune disease is strongly linked with coeliac’s?

A

Type 1 diabetes

106
Q

How is coeliac’s diagnosed?

A

Anti TTG antibodies and histology shwoing villous atrophy and crypt hypertrophy

107
Q

How does appendicitis present?

A

Central abdominal pain which moves down to the right iliac fossa within 24 hours, becoming localised there

108
Q

At which anatomical landmark can tenderness be identified in appendicitis?

A

McBurney’s point (one third of the distance from the ASIS to the umbilicus)

109
Q

What is rovsig’s sign?

A

palpation of the left iliac fossa causes pain in the RIF

110
Q

Which 3 signs potentially indicate a ruptured appendix?

A

Rebound tenderness
Percussion tenderness
Pertitonitis

111
Q

How is appendicitis diagnosed?

A

Diagnosis is based on the clinical presentation and raised inflammatory markers

CT and ultrasound can aid a diagnosis

Diagnosis is confirmed by a diagnostic laparoscopy

112
Q

What is an appendix mass?

A

When the omentum surrounds and sticks to the inflammed appendix

113
Q

What is the management of appendicitis?

A

Appendicectomy by laparoscopic surgery

114
Q

What is third-spacing?

A

The abnormal loss of fluid from the intravascular space into the GI tract

115
Q

What are the “big three” causes for bowel obstruction?

A

Adhesions
Hernia
Malignancy

116
Q

What is a closed loop obstruction?

A

There are two points of obstruction along a bowel meaning that there is a middle section which will continue to expand leading to ischaemia and perforation

117
Q

What is the presentation of bowel obstruction?

A

Vomiting (green and bilious)
Abdominal distention
Diffuse abdominal pain
Absolute constipation and lack of flactulance
Tinkling bowel sounds

118
Q

What is the finding in an abdominal x-ray of bowel obstruction?

A

Distended loops of bowel

119
Q

What may be seen on venous blood gas of someone with bowel obstruction?

A

Metabolic alkalosis

120
Q

What can be seen on erect chest x-ray of bowel perforation

A

Air under the diaphragm

121
Q

What is the definitive management of bowel obstruction?

A

Exploratory surgery
Adhesiolysis
Hernia repair
Emergency resection

122
Q

What is ileus?

A

A condition which affects the small bowel where peristalsis stops and causes a pseudo-obstruction (functional obstruction)

123
Q

What are common causes of ileus?

A

Injury
Handing of the bowel during surgery
Inflammation or infection
Electrolyte imbalance

124
Q

What are the symptoms of ileus?

A

Similar to bowel obstruction

Green vomiting
Abdominal distention
Absolute constipation and lack of flatulence

125
Q

What is the management of ileus?

A

Nil by mouth
NG tube if vomiting
IV fluid

126
Q

What is volvulus?

A

When the bowel twists around itself and the mesentery that it is attached to. This leads to a closed-loop bowel obstruction which leads to ischaemia

127
Q

What are the two main types of volvulus?

A

Sigmoid volvulus and caecal volvulus

128
Q

What is a sigmoid volvulus?

A

Twist in the sigmoid colon. Caused by chronic constipation. High association with a high fibre diet and excessive use of laxatives

129
Q

What is the presentation of volvulus?

A

Same as bowel obstruction (again)

130
Q

How is volvulus diagnosed?

A

Abdominal x-ray shows the coffee bean sign

Contrast CT is the diagnostic test

131
Q

How is volvulus managed?

A

Conservative management (endoscopic decompression)

Laparotomy
Hartmann’s procedure

132
Q

What are the 3 complications of hernias?

A

Incarceration
Obstruction
Strangulation

133
Q

What is incarceration of a hernia?

A

A hernia cannot be reduced (stuck in the mud)

134
Q

What is strangulation of a hernia?

A

Where a hernia is non-reducible and the base of the hernia becomes so tight that it cuts of the blood supply

135
Q

What are the 3 management options for hernias?

A

Conservative
Tension-free repair
Tension repair

136
Q

What is the difference between direct and indirect inguinal hernias?

A

An indirect hernia is when the bowel herniates through the inguinal canal.

A direct hernia occurs due to weakness in the abdominal wall at Hesselbach’s triangle

137
Q

What are femoral hernias?

A

Herniation of the abdominal contents through the femoral canal. This occurs below the inguinal ligament

138
Q

How do you differentiate between direct and indirect inguinal hernias?

A

If you reduce an indirect inguinal hernia and place pressure at the deep inguinal ring (half way between the ASIS and the pubic tubercle) then it will remain reduced as a direct will not.

139
Q

What are obturator hernias?

A

When the abdominal or pelvic contents herniate through the obturator foramen. Usually happens due to defect in the pelvic floor

140
Q

What is the sign indicative of a obturator hernia?

A

Howhip-Romberg sign= pain extending from the inner thigh to knee when the internally rotated

141
Q

What is a hiatus hernia?

A

Herniation of the stomach through the diaphragm

142
Q

What are haemorrhoids?

A

Enlarged anal vascular cushions

143
Q

What are haemorrhoids usually associated with?

A

Pregnancy, obesity, increased age, increased intra-abdominal pressure (weightlifting or chronic coughing)

144
Q

Where do anal cushions get their blood supply?

A

Rectal arteries

145
Q

How do you classify haemorrhoids?

A

1st degree= no prolapse
2nd degree= prolapse on straining, return on relaxing
3rd degree= no return on relaxing but can be pushed back
4th degree= permenantly prolapsed

146
Q

How are haemorrhoids diagnosed?

A

PR
Protoscopy

147
Q

How are haemorrhoids managed?

A

Anusol (contains astringents which shrink the haemorrhoid)
Anusol HC (+hydrocortisone)

Increasing fibre in diet and fluid intake

Rubber band ligation or injection sclerotheraoy

Haemorrhoid artery ligation

Haemorrhoidectomy

148
Q

How do thrombosed haemorrhoids present?

A

VERY pain
appear purplish, very tender and swollen

149
Q

What is diverticulosis?

A

Refers to the presence of diverticula, without inflammation or infection

150
Q

What is diverticulitis?

A

Refers to the inflammation and infection of diverticula

151
Q

How is diverticulosis managed?

A

The patient is often asymptomatic

If there are symptoms (lower left abdo pain and constipation) then try bulk-forming laxatives (isaghula husk). AVOID stimulant laxatives

152
Q

How does acute diverticulitis present?

A

Pain and tenderness in the LIF
Fever
Diarrhoea
N+V
rectal bleeding

153
Q

What is the management of acute diverticulitis?

A

Oral co-amoxiclav
Analgesia

If severe then admit. IV fluids. abx and CT. May need surgery for complications

154
Q

What is the blood supply of the foregut?

A

Coeliac artery

155
Q

What is the blood supply of midgut?

A

Superior mesenteric artery

156
Q

What is the blood supply of the hindgut?

A

Inferior mesenteric artery

157
Q

How does chronic mesenteric ischaemia present?

A

Colicky abdominal pain after eating
Weight loss
Abdominal bruit

158
Q

How is chronic mesenteric ischaemia diagnosed?

A

CT angiography

159
Q

What is the management of chronic mesenteric ischaemia?

A

Reducing modifiable risk factors
Secondary prevention
Revascularisation

160
Q

What tends to cause acute mesenteric ischaemia?

A

Thrombus in the superior mesenteric artery (may be secondary to AF)

161
Q

What is the diagnostic test for acute mesenteric ischaemia?

A

Contrast CT

162
Q

What effect does bowel ischaemia have on the bloods?

A

metabolic acidosis
raised lactate

163
Q

What is familial adenomatous polyposis?

A

Autosomal dominant disorder which causes the malfunctioning of the tumour suppressor genes which results in polyps (adenomas) developing along the large intestine

164
Q

What is the management of familial adenomatous polyposis?

A

Patients usually have the whole large bowel removed prophylactically because there is a high chance that the polyps will become malignant

165
Q

What is lynch syndrome and what is it’s inheritance pattern?

A

Hereditary nonpolyposis colorectal cancer

166
Q

What are the red flags for bowel cancer?

A

Change in bowel habit
Unexplained weight loss
Rectal bleeding
Unexplained abdominal pain
Iron deficiency anaemia
Abdominal or rectal mass

167
Q

What is the screening programme for bowel cancer?

A

faecal immunochemical test (FIT).

people between 60 and 74 are sent a FIT test to do every 2 years, if positive they are sent for a colonoscopy

168
Q

What is the gold standard test for bowel cancer?

A

Colonoscopy with biopsy

169
Q

What are the stages of TNM classifcation?

A

T=tumour
Tx- unable to assess size
T1-submucosa involvement
T2-involvement of the muscularis propria
T3- involvement of the subserosa and serosa
T4- spread through the serosa (a) reaching other organs (b)

N= nodes
NX= unable to assess nodes
N0= no nodal spread
N1= spread to 1-3 nodes
N2= spread to more than 3 nodes

M= metastasis
M0= non metastasis
M1= metastasis

170
Q

What are most gallstones made out of?

A

Cholesterol

171
Q

What are the risk factors for gallstones?

A

The 4 Fs:
Fat
Fair
Female
Forty

172
Q

How do gallstones present?

A

Biliary colic (severe, epigastric or RUQ pain)
Often triggered by meals
Lasts between 30 mins and 8 hours
May be associated with nausea and vomiting

173
Q

What is the first line investigation for gallstones?

A

Ultrasound

174
Q

Which scan should be used to investigate gallstones if ultrasound shows nowt?

A

MRCP

175
Q

What is used to clear stones in bile ducts?

A

ERCP

176
Q

What is acute cholecystitis?

A

Inflammation of the gallbladder

177
Q

What is acute cholangitis

A

Inflammation of the bile ducts

178
Q

What is the presentation of acute cholecystitis?

A

RUQ pain which radiates to the right shoulder

Fever
Tachycardia
Vomiting
Murphy’s sign
Raised inflammatory markers

179
Q

Which sign is suggestive of acute cholecystitis?

A

Murphy’s sign

Hand on RUQ, ask to breathe in, stimulation of the acute gallbladder will suddenly stop inspiration

180
Q

How should patients with acute cholecystitis be managed?

A

Nil by mouth
IV fluids
Abx
NG tube
ERCP for stones
Cholecystectomy within 1 week

181
Q

How does acute cholangitis present?

A

Charcot’s triad:
RUQ pain
Fever
Jaundice

182
Q

How is acute cholangitis managed?

A

ERCP
PTC (percutaneous transhepatic cholangiogram)

183
Q

What are the 2 most probable diagnoses when there is painless jaundice?

A

Cholangiocarcinoma
Pancreatic cancer

184
Q

What is the tumour marker for cholangiocarcinoma and pancreatic adenocarcinoma?

A

CA19-9

185
Q

What are the referral criteria for pancreatic cancer?

A

Over 40 with jaundice (2 week wait)

Over 60 with jaundice and any of:
Diarrhoea
Back pain
Abdominal pain
Nausea
Vomiting
Constipation
New onset diabetes

For direct access CT abdo

186
Q

What is trousseau’s sign of malignancy and which cancer is it suggestive of?

A

Migratory thrombophlebitis

Pancreatic adenocarcinoma

187
Q

What is a whipple procedure?

A

Pancreaticoduodenectomy

188
Q

What are the 3 main causes of pancreatitis?

A

Gallstones
Alcohol
Post-ERCP

189
Q

What are the causes of pancreatitis?

A

I GET SMASHED

I- idiopathic
G- Gallstones
E- ethanol
T- trauma
S- Steroids
M- mumps
A- autoimmune
S- Scorpion stings!!
H- hyperlipidaemia
E- ERCP
D- Drugs

190
Q

What is the presentation of acute pancreatitis?

A

Severe epigastric pain which radiates through the back
Associated vomiting
Abdominal tenderness
Systemically unwell

191
Q

What is seen on bloods in acute pancreatitis?

A

Amylase & Lipase (more specific)
CRP
Ultrasound
CT abdomen

192
Q

Which score is used to assess the severity of pancreatitis?

A

Glasgow

0 or 1= mild
2= moderate
3 or more= severe

193
Q

What is the presentation of chronic pancreatitis?

A

Chronic epigastric pain
Loss of exocrine function (lack of pancreatic enzymes)
Loss of endocrine function ( o diabetes)

194
Q

How is chronic pancreatitis managed?

A

Abstinence from alcohol and smoking
Analgesia
Replacement pancreatic enzymes (creon)
Sub cut insulin
ERCP with stenting
Surgery

Alice's finals cards (23 decks)

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