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MLA Gastro Flashcards

1
Q

What is acute cholangitis?

A

Infection of the biliary tree

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2
Q

What is the clinical presentation of biliary colic?

A

Sudden onset, severe, colicky RUQ pain
Often preceded by fatty meal
Systemically well

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3
Q

How is biliary colic diagnosed?

A

Abdominal ultrasound

No raised inflammatory markers or abnormal LFT’s

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4
Q

What is the management for biliary colic?

A

Passes itself so only simple analgesia
Avoid triggers: weight loss, low-fat diet, avoid fatty meals

If recurrent, offer elective laparoscopic cholecystectomy

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5
Q

What is acute cholecystitis?

A

Acute inflammation of the gallbladder, usually secondary to gallstones

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6
Q

What is the clinical presentation of acute cholecystitis?

A

Preceded by biliary colic, but now the pain is more constant in the RUQ and radiates to the epigastrium and right shoulder

Worse on deep inspiration
Positive Murphey’s test

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7
Q

How is acute cholecystitis diganosed?

A

Bloods: increased WCC and CRP. deranged LFT’s
Ultrasound will show obstruction usually by gallstone and associated gallbladder wall inflammation

If sepsis is suspected, request contrast CT or MRI to look for abdominal pathologies, gangrenous cholecystitis or perforations

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8
Q

How is acute cholecystitis managed?

A

Requires hospital admission for antibiotics and laparoscopic cholecystectomy

Offer percutaneous cholecystostomy (catheter) if patient unable to tolerate general anaesthesia due to frailty of comorbidities

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9
Q

What is percutaneous cholecystostomy?

A

When a catheter is inserted into the gallbladder to drain the contents

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10
Q

What is acute cholangitis?

A

Acute bacterial infection of the biliary tree (most severe complication of gallstones)

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11
Q

What is the difference between ERCP and MRCP?

A

MRCP: Magnetic resonance cholangiopancreatography (just an MRI)

ERCP: Endoscopic retrograde cholangiopancreatography (endoscope goes down oesophagus and into the biliary tree)

MRCP doesn’t require anaesthesia and has minimal risk but can’t treat anything in the moment

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12
Q

What is the difference between ascending cholangitis and acute cholangitis?

A

Same thing

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13
Q

What is the clinical presentation of ascending cholangitis?

A

Pale stools, dark urine, and concurrent sepsis

Charcot’s triad: RUQ pain, jaundice, fever

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14
Q

What investigations need to be done for acute cholangitis?

A

Blood will show elevated CRP, WCC, deranged LFT’s
Some patients will develop thrombocytopenia, coagulopathies, and raised lactate

Ultrasound will show dilated bile ducts

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15
Q

How is acute cholangitis diagnosed?

A

ERCP is gold standard but invasive so MRCP is often done instead

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16
Q

How is acute cholangitis managed?

A

Antibiotics
Correct electrolyte or coagulation disturbances

ERCP first-line to decompress gallbladder or Percutaneous trans-hepatic cholangiography (PTC) if patient unable to tolerate general anaesthesia

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17
Q

What is the pathophysiology of acute pancreatitis?

A

Hypersecretion or backflow of digestive enzymes leading to autodigestion

Most common causes: gallstones and alcohol
Other: idiopathic, trauma, steroids, malignancy, autoimmune disease, ERCP

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18
Q

What is the clinical presentation of acute pancreatitis?

A

Epigastric tenderness
Abdominal distention
Reduced bowel sounds
Fever, hypotension, tachycardia

Cullen’s sign: periumbilical bruising
Grey-Turner’s sign: flank bruising
(Both signs of haemorrhagic pancreatitis)

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19
Q

What are some complications of pancreatitis?

A

Early:
Necrotising pancreatitis
Necrosis
Abscess
acute respiratory distress syndrome (ARDS)

Late:
Pseudocyst
Portal vein/splenic thrombosis
Chronic pancreatitis
Pancreatic insufficiency

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20
Q

How is acute pancreatitis diagnosed?

A
  1. Abdominal pain and history suggestive of acute pancreatitis
  2. Serum amylase/lipase over 3x the normal limit
  3. Imaging findings
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21
Q

What imaging investigations are done for pancreatitis?

A

Erect chest x-ray: looks for free gas under the diaphragm resulting from ischaemia, erosion, infection, mechanical injury

CT abdo pelvis: excludes complications like pseudocyst formation

Abdo ultrasound: assesses biliary tree for obstruction

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22
Q

How is the severity of pancreatitis assessed?

A

Glasgow-Imrie score

PaO2 <7.9
Age >55
Neutrophils (really WCC) >15
Calcium <2.0
Renal function: urea >16mmol/L
Enzymes: LDH >600 IU/L
Albumin <32 g/L
Sugar >10mmol

or Ranson’s criteria to predict mortality from pancreatitis

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23
Q

How is acute pancreatitis managed?

A

Fluid resuscitation
Analgesia
Antiemetics
Nill by mouth
Control blood glucose

Gallstone related: ERCP or cholecystectomy
Alcohol induced: withdrawal

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24
Q

How is an anal fissure managed?

A

-Diet/meds to soften stool
-Sitz bath after bowel movements
-Topical anaesthetics Eg. lidocaine
-Topical vasodilators Eg. nifedipine or nitroglycerin to relax anal sphincter muscles

Chronic fissures:
Offer botox injections or surgery

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25
What are the different causes of ascites?
Most common: liver cirrhosis Other: cancer, heart disease, pancreatitis, low protein levels, portal hypertension
26
What is the difference between exudate and transudate?
Exudate: tissue leakage due to inflammation or local cellular damage. Contains cells, proteins, and solid materials Transudate: Caused by systemic conditions that alter pressure in vessels. Contains low proteins. Just a watery solution
27
What is the most common type of colorectal tumour?
Adenocarcinoma - Starts in the cells that line the colon and rectum
28
What is non-alcoholic fatty liver disease?
AKA steatohepatitis Caused by a build up of fat in the liver by obesity, diabetes, high cholesterol, or high bp Management: life style changes
29
What is the clinical presentation of non-alcoholic fatty liver disease?
Fatigue Upper abdominal pain Hepatomegaly Often without symptoms
30
What is the pathophysiology of liver cirrhosis?
Fibrosis and nodule formation caused by liver injury lead to alterations in the normal lobar organisation of the liver
31
How does liver disease cause palmar erythema?
Abnormal estradiol levels activate nitric oxide synthase, which produces nitric oxide and causes vasodilation
32
How does liver disease lead to sex hormone imbalances?
Liver can't break down oestrogen causing increasing levels Also as liver disease progresses, the liver's ability to transform testosterone and estrone into estradiol increases. This can lead to reduced androgen secretion by the testicles
33
What is sarcopenia?
Muscle loss
34
How does platelet count link with liver disease?
Direct correlation Liver produces thrombopoietin, less is made in diseased liver so the bone marrow is stimulated less
35
What is ACLF?
Acute on chronic liver failure Sudden decompensation in pre-existing liver disease Precipitated by infections like hep B, alcohol use, gastro haemorrhage, or drugs
36
What is included in liver function tests?
- Albumin - Total protein - Alkaline phosphatase (ALP) - Alanine transaminase (ALT) - Aspartate transaminase (AST) - Gamma-glutamyl transferase (GGT) - Bilirubin - Prothrombin time (PT)
37
What causes Alkaline phosphatase (ALP) levels to be deranged?
Produced in liver epithelial cells and bones - If high, suggests interruption to bile flow from hepatocytes (Eg, gallstones) or bone disease or bone growth (Eg Kids) - Linked with heart failure
38
What causes deranged alanine transaminase (ALT)?
Indicates liver cell damage - Very specific to liver damage Caused by hepatitis, cirrhosis, cancer, medications, alcohol excess, fatty liver, hemochromatosis, ischaemia, pancreatitis
39
What is the FIB-4 index?
Determines risk of liver fibrosis using age, AST, ALT, and platelet count
40
What causes deranged Aspartate transaminase (AST)?
Indicates liver damage but also elevated after cardiac muscle damage and other tissues Less specific that ALT
41
What is the difference between AST and ALT?
Both suggest liver damage but ALT is more specific to liver, as AST is in cardiac muscles too
42
What causes deranged gamma-glutamyl transferase (GGT)?
Indicates damage to the liver and bile ducts. Interpreted alongside ALP - High ALP, normal GGT: bone disease (EG. Paget's disease) - High ALP, high GGT: cholestasis - High GGT only: alcohol excess
43
What is the AST: ALT ratio?
Helps determine the aetiology of hepatocellular injury 2:1 ratio is classic for alcoholic liver disease
44
How is bilirubin metabolised?
- RBC's are broken down, and unconjugated (insoluble) bilirubin is created which binds to albumin - Hepatocytes metabolise it into conjugated (soluble) bilirubin and excrete it into biliary tract where it flow as bile - Gut bacteria metabolise bile into urobilinogen and it's excreted as stercobilnigen, giving it the dark colour - Some urobilinogen is water-soluble and the kidney is able to excrete this in urine
45
What is the BASL bundle?
Helps with management of decompensated chronic liver disease Includes: - Basic investigations like LFT's - Alcohol intake Q's - Ascitic tap - Albumin and CRP - Urine dip - CXR, USS abdo
46
What are the characteristics of melaena?
Jet black Sticky consistency Difficult to flush Offensive smell
47
Which LFT's will suggest acute hepatocellular damage?
Very high ALT and AST Others may be slightly high or normal
48
Which LFT's suggest cholestasis?
Very high ALP and GGT Others may be slightly high or normal
49
What are the different types and causes of diarrhoea?
Bloody: caused by IBD, infective colitis, ischaemic colitis Secretory: viral infection, C.diff, carcinoid syndrome, neuroendocrine tumours Fatty/ malabsorption: coeliac, chronic pancreatitis, bile salt malabsorption Osmotic: laxatives
50
What is the Child-Pugh score for?
To assess the severity of liver disease and predict mortality in patients with cirrhosis
51
What is diverticular disease?
When there are pouches pushing out of the large intestine where it's weaker Risks: genetics, low-fibre diet, lack of physical activity, obesity, connective tissue issues, meds like NSIADs, alcohol
52
What are the consequences of a hiatus hernia?
GORD, stomach ulcers, strictures, lung infections, bleeds, bowel changes like constipation
53
What is the management of a hiatus hernia?
1st line: lifestyles changes to manage symptoms and meds like antacids and antihistamines 2nd line: surgery if nothing else works. Eg. magnetic sphincter augmentation to strengthen the lower oesophageal sphincter
54
What are the consequences of a splenectomy?
- Susceptibility to serious infections like pneumonia, influenza, haemophilus influenzae type b, meningicocci so patients need long tern vaccines and antibiotics - Blood clots and destruction of RBC's - Increased risk of cancer in first 2-5 years after surgery - Abdominal wall hernia
55
What are the consequences of infectious mononucleosis infection?
AKA glandular fever by Epstein-Barr virus - Causes enlargement of the spleen and hepatitis - May lead to encephalitis, meningitis, seizures, kidney inflammation, and haemolytic anaemia - In immunocompromised, can cause Hodgkin's lymphoma and nasopharyngeal carcinoma
56
Who is most likely to present with infectious mononucleosis?
Teenagers and young adults at university
57
What are the symptoms of infectious mononucleosis?
Extreme fatigue Fever Sore throat Headaches and body aches Lymphadenopathy Enlarged liver and spleen Rash Symptoms appear 2-4 weeks after infection and last about 1-6 months
58
What is mesenteric adenitis?
Swelling of the lymph nodes in the mesentery Symptoms: Pain in RIF, fever, vomiting, diarrhoea, nausea, reduced appetite, fatigue, general abdominal tenderness - Commonly mistaken for appendicitis Affects mostly children and teenagers
59
What is necrotising enterocolitis?
Intestinal inflammation that causes tissue necrosis Most common in 2nd or 3rd week of life and more often in premature babies
60
How does necrotising enterocolitis present?
Swollen, tender belly red, blue,, or grey abdo discolouration Bowel habit changes lethargy Low/ unstable body temp
61
What is the pathophysiology of necrotising enterocolitis?
The intestine is immature and doesn't have an adequate barrier against bacteria yet
62
How can necrosing enterocolitis be prevented?
- Breast feeding - Antenatal corticosteroids in preterm - Probiotics - Prevent anaemia, supressing gastric acid secretion, and long term antibiotic use
63
What is the management of hemochromatosis?
- Venesection and chelation therapy help manage iron levels - Screening for liver disease Prognosis best if diagnosed early
64
What is a SAAG score?
Serum-ascites albumin gradient (SAAG) >1.1(high) indicates a nonperitoneal cause of ascites, such as cirrhosis, fulminant hepatic failure, or congestive heart failure A low SAAG score (<1.1) is more from malignancy or infection
65
What are the features of autoimmune hepatitis?
Hepatomegaly Jaundice Fatigue Abdominal pain
66
What are smooth muscles antibodies?
Autoantibodies that mainly attack the liver High in autoimmune hepatitis
67
How does the drug Azathioprine work?
An immunosuppressant often used for long term control of autoimmune conditions and initial steroid therapy
68
What is primary biliary cholangitis?
AKA primary biliary cirrhosis Autoimmune and mostly happens in middle-aged women Progressively gets worse leading to liver failure Presents with lethargy and pruritis
69
What is the management of primary biliary cholangitis?
Ursodeoxycholic acid prevents progression Cholestyramine alleviates pruritus but must be given at least 2 hours apart from ursodeoxycholic acid Ultimately patients may need transplantation

Year 5 (23 decks)

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