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Year 5 > MLA Gastro > Flashcards

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
Q

What are the different causes of ascites?

A

Most common: liver cirrhosis

Other: cancer, heart disease, pancreatitis, low protein levels, portal hypertension

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26
Q

What is the difference between exudate and transudate?

A

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

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27
Q

What is the most common type of colorectal tumour?

A

Adenocarcinoma
- Starts in the cells that line the colon and rectum

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28
Q

What is non-alcoholic fatty liver disease?

A

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
Q

What is the clinical presentation of non-alcoholic fatty liver disease?

A

Fatigue
Upper abdominal pain
Hepatomegaly

Often without symptoms

30
Q

What is the pathophysiology of liver cirrhosis?

A

Fibrosis and nodule formation caused by liver injury lead to alterations in the normal lobar organisation of the liver

31
Q

How does liver disease cause palmar erythema?

A

Abnormal estradiol levels activate nitric oxide synthase, which produces nitric oxide and causes vasodilation

32
Q

How does liver disease lead to sex hormone imbalances?

A

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
Q

What is sarcopenia?

A

Muscle loss

34
Q

How does platelet count link with liver disease?

A

Direct correlation

Liver produces thrombopoietin, less is made in diseased liver so the bone marrow is stimulated less

35
Q

What is ACLF?

A

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
Q

What is included in liver function tests?

A
  • Albumin
  • Total protein
  • Alkaline phosphatase (ALP)
  • Alanine transaminase (ALT)
  • Aspartate transaminase (AST)
  • Gamma-glutamyl transferase (GGT)
  • Bilirubin
  • Prothrombin time (PT)
37
Q

What causes Alkaline phosphatase (ALP) levels to be deranged?

A

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
Q

What causes deranged alanine transaminase (ALT)?

A

Indicates liver cell damage
- Very specific to liver damage

Caused by hepatitis, cirrhosis, cancer, medications, alcohol excess, fatty liver, hemochromatosis, ischaemia, pancreatitis

39
Q

What is the FIB-4 index?

A

Determines risk of liver fibrosis using age, AST, ALT, and platelet count

40
Q

What causes deranged Aspartate transaminase (AST)?

A

Indicates liver damage but also elevated after cardiac muscle damage and other tissues

Less specific that ALT

41
Q

What is the difference between AST and ALT?

A

Both suggest liver damage but ALT is more specific to liver, as AST is in cardiac muscles too

42
Q

What causes deranged gamma-glutamyl transferase (GGT)?

A

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
Q

What is the AST: ALT ratio?

A

Helps determine the aetiology of hepatocellular injury

2:1 ratio is classic for alcoholic liver disease

44
Q

How is bilirubin metabolised?

A
  • 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
Q

What is the BASL bundle?

A

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
Q

What are the characteristics of melaena?

A

Jet black
Sticky consistency
Difficult to flush
Offensive smell

47
Q

Which LFT’s will suggest acute hepatocellular damage?

A

Very high ALT and AST

Others may be slightly high or normal

48
Q

Which LFT’s suggest cholestasis?

A

Very high ALP and GGT

Others may be slightly high or normal

49
Q

What are the different types and causes of diarrhoea?

A

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
Q

What is the Child-Pugh score for?

A

To assess the severity of liver disease and predict mortality in patients with cirrhosis

51
Q

What is diverticular disease?

A

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
Q

What are the consequences of a hiatus hernia?

A

GORD, stomach ulcers, strictures, lung infections, bleeds, bowel changes like constipation

53
Q

What is the management of a hiatus hernia?

A

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
Q

What are the consequences of a splenectomy?

A
  • 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
Q

What are the consequences of infectious mononucleosis infection?

A

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
Q

Who is most likely to present with infectious mononucleosis?

A

Teenagers and young adults at university

57
Q

What are the symptoms of infectious mononucleosis?

A

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
Q

What is mesenteric adenitis?

A

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
Q

What is necrotising enterocolitis?

A

Intestinal inflammation that causes tissue necrosis

Most common in 2nd or 3rd week of life and more often in premature babies

60
Q

How does necrotising enterocolitis present?

A

Swollen, tender belly
red, blue,, or grey abdo discolouration
Bowel habit changes
lethargy
Low/ unstable body temp

61
Q

What is the pathophysiology of necrotising enterocolitis?

A

The intestine is immature and doesn’t have an adequate barrier against bacteria yet

62
Q

How can necrosing enterocolitis be prevented?

A
  • Breast feeding
  • Antenatal corticosteroids in preterm
  • Probiotics
  • Prevent anaemia, supressing gastric acid secretion, and long term antibiotic use
63
Q

What is the management of hemochromatosis?

A
  • Venesection and chelation therapy help manage iron levels
  • Screening for liver disease

Prognosis best if diagnosed early

64
Q

What is a SAAG score?

A

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
Q

What are the features of autoimmune hepatitis?

A

Hepatomegaly
Jaundice
Fatigue
Abdominal pain

66
Q

What are smooth muscles antibodies?

A

Autoantibodies that mainly attack the liver

High in autoimmune hepatitis

67
Q

How does the drug Azathioprine work?

A

An immunosuppressant often used for long term control of autoimmune conditions and initial steroid therapy

68
Q

What is primary biliary cholangitis?

A

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
Q

What is the management of primary biliary cholangitis?

A

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 (16 decks)

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