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YR3 - R1: General Medicine > Gastroenterology & Shock > Flashcards

Gastroenterology & Shock Flashcards

1
Q

What are the 2 basic functions of the liver?
What are the 3 basic pathophysiological pathways of liver disease?

A

Liver Function - Synthetic & Excretory
2 causes of acute liver failure = Hep A & Paracetamol overdose
Chronic = alcohol, hepatitis B

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2
Q

Surgical sieve for causes of liver disease?
- Toxic?
- Infections?
- Metabolic/Genetic?
- Inflammatory/Autoimmune?
- Vascular?
- Neoplasia?
- Trauma?
- Idiopathic?
- Biliary Tract Disease?

A
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3
Q

What are the 3 main complications of liver disease?

A
  • Liver stops detoxifying = encephalopathy = acute confusional state due to liver failing and build up of toxins
  • Vitamin K clotting factors made by the liver = bleeding
  • Portal-systemic system anastomoses at the distal esophagus, anus, umbilical region = varices due to pressure pushing back
  • Ascites - think: Liver failure & Malignancy & Nephrotic syndrome & Severe HF
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4
Q

Isolated ALP?

A
  • Is the problem with in the liver cells or is there a bile duct obstruction?
  • Hepatocellular cells aren’t working so won’t respond to Vitamin K – ie. Wont make more vitamin K dependent factors
  • Isolated ALP – think bone disorders & bony METS!
  • If ALP raised, look at the Gamma GT – if its raised = liver, if it’s not = bone (eg. Pagets)
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5
Q

List 10 Signs of Chronic Liver Disease?
List 3 signs of chronic liver disease in the setting of alcoholism?

A
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6
Q

5 Signs of Acute Hepatic Failure?

A
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7
Q

Describe a clinical approach to liver disease? 4 questions to ask yourself?
- 4 things that can precipitate an acute encephalopathy in a patient with chronic liver disease?

A
  • Always assume bacterial peritonitis in a patient with hepatic encephalopathy ALSO consider their bleeding risk.
  • Propranolol used to reduce risk of bleed in patients with varices.
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8
Q

Outline hx, exam and ixs of suspected liver disease?

A
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9
Q

What are 5 general lab tests you should perform for a patient with suspected liver disease? Why?

A
  • You want a full blood picture because you want to know if they’ve bled plus if alcohol abuse = low white cell count (bone marrow suppressed) and hypersplenism = low platelet count.
  • You want a coag profile to see what their clotting ability is like
  • U&Es – want to know if they are gonna tip into encephalopathy & renohepatic syndrome/what are their kidneys doing + if they’ve bled their urea will be up in proportion to their creatinine.
  • Culture – blood/urine – infection?
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10
Q
  • Which biomarker will assess the excretory function of the liver?
  • Which biomarkers will assess the synthetic function of the liver? (3)
  • Which biomarkers will assess hepatocellular damage? (2)
  • Which biomarkers will assess bile duct obstruction? (2)
A
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11
Q

List 3 special tests of function you would consider in suspected liver disease other than LFTs/routine bloods?

A

Failure to clear ammonia = why they become encephalopathic
Other viruses – EBV, CMV

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12
Q
  • Which metabolic markers might you test in suspected liver disease? (3)
  • Which immunological markers might you test in suspected liver disease? (2)
  • Which tumour marker might you test in suspected liver disease? (1)
A

Iron (haemochromatosis), copper (Wilsons), primary hepatocellular carcinoma (alpha-fetoprotein tumour marker will go up).

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13
Q

List 8 Imaging modalities you might consider in a patient with suspected liver disease?

A

If you suspect Budd-Chiari/obstruction of portal vein = Ultrasound

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14
Q

2 serological tests for Hep A and the meaning of a positive result?

A
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15
Q

6 serological tests for Hep B and the meaning of a positive result?

A
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16
Q
  • 2 serological tests for Hep C and the meaning of a positive result?
  • 2 serological tests for Hep D and the meaning of a positive result?
  • 1 serological tests for Hep E and the meaning of a positive result?
A
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17
Q

5 Other infections to test for other than Hepatitis virus in patients with suspected liver disease?

A
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18
Q

5 Tests to consider for autoimmune liver disease and what a positive result means?

A
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19
Q

6 Tests to consider for autoimmune liver disease and what a positive result means?

A
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20
Q

What is GERD according to the Montreal classification: Consensus Statement?
- Epidemiology?

A
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21
Q

List 9 Classical Symptoms of GERD?

A
  1. Heartburn
  2. Regurgitation of acid and food
  3. Burping
  4. Postprandial symptoms
  5. Dysphagia
  6. Odynophagia
  7. Nocturnal symptoms – cough
  8. Exercise induced regurgitation
  9. Waterbrash
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22
Q

List 8 Atypical Reflux presentations?

A

Infections – esophageal candida – eg. Asthma preventors

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23
Q

List 6 conditions GERD is associated with?
- CREST?

A
  1. Hiatus hernia
  2. Scleroderma / Crest syndrome
  3. Bed bound patients
  4. Post op – prolonged NG tube feed
  5. MVA – diaphragm injuries
  6. Bulaemia
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24
Q

List 6 Any Alarm symptoms of GERD that are indications for Gastroscopy?

A
  1. Dysphagia
  2. Odynophagia
  3. GIT bleeding – haematemesis and melaena
  4. Anaemia
  5. Weight loss
  6. Recurrent vomiting
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25
Q

What is considered a Mild GERD? Management? (4)

A
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26
Q

When is GERD considered to be Moderate to Severe? Management?

A

GERD: Moderate to Severe
- Persistent symptoms, often daily, needing antacids regularly and not responding adequately to H2 receptor antagonists
- Trial of a PPI – omeprazole, esomeprazole pantoprazole, rabreprazole or lansoprazole.
- If inadequate response to 4 to 6 weeks treatment and symptoms recur - gastroscopy
- Domperidone = increased gastric emptying

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27
Q

What are 4 things to do during/look for during gastroscopy for reflux?

A
  1. Assess for oesophagitis
  2. Los Angeles Grading
  3. ?Barrett’s present –biopsies
  4. Any other pathology - helicobacter
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28
Q

Describe the Los Angeles Grading System for GERD - Grade A?

A
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29
Q

Describe the Los Angeles Grading System for GERD - Grade B?

A
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30
Q

Describe the Los Angeles Grading System for GERD - Grade C?

A
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31
Q

Describe the Los Angeles Grading System for GERD - Grade D?

A
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32
Q

Discuss the role of PPIs as a long term medication for GERD?
- Safety?
- Metabolism?
- Common adverse effects?
- Potential interactions?
- Very rare adverse effects? (4)

A
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33
Q

List 5 Long term concerns with PPIs?

A

PPIs increase beta-amyloid = dementia?

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34
Q

List 5 INDICATIONS FOR PPIs?

A
  1. Peptic Ulcer (treat Helicobacter)
  2. Erosive Oesophagitis
  3. Chronic NSAID’s use
  4. NSAID’s and anticoagulation – aspirin , clopidogrel, warfarin, new anticoagulants. Greater risk of GIT bleed with increasing age.
  5. Barrett’s oesophagus
    THINK about cost and indications
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35
Q

When should you cease PPI use?

A
  • Mild reflux may resolve
  • Elderly- more likely severe oesophagitis and milder symptoms –don’t stop
  • Balance: PPI’s have changed management of severe reflux and oesophageal strictures.
  • Think about the indications and is it appropriate
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36
Q

When would you consider Antireflux surgery in a patient with GERD? (5)
What is this surgery called?

A
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37
Q

Which 2 studies must you perform prior to Antireflux surgery (Laparoscopic fundoplication) and why?

A

pH AND MOTILITY STUDIES
- Use pre surgery to confirm normal motility
- If uncertain about reflux and symptoms – NERD but “sensitive “ oesophagus. Difficult clinical scenario. Mechanism poorly understood
- Atypical chest pain
- Motility disorders -achalasia

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38
Q

Describe an algorithm of the medical management of GERD?

A
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39
Q

What is BARRETT’S OESOPHAGUS (BO)? What is it associated with? Risk of oesophageal adenocarcinoma?

A
  • Definition: The replacement of stratified squamous epithelium with specialised intestinal metaplastic columnar epithelium within the tubular oesophagus.
  • Associated with chronic GERD.
  • Increased risk of Oesophageal adenocarcinoma 30x the average population.
  • ABSOLUTE RISK IS LOW
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40
Q

Describe the epidemiology of Barrett’s esophagus?

A
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41
Q

Which Classification system is used to describe Barretts oesophagus?

A
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42
Q

List 7 High risk groups for Barrett’s Oesophagus?

A
  1. Chronic reflux –GERD
  2. Hiatus hernia
  3. Males over 50
  4. White
  5. Smokers
  6. Obese, high BMI, central obesity
  7. Family history oesophageal cancer or BO
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43
Q

Do we routinely screen for Barrett’s? Conversion rate?

A
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44
Q

What should you do if Barrett’s esophagus is present? (4)

A
  1. Control reflux – high dose PPI controls reflux but no current evidence prevents cancer
  2. Careful follow up of high risk group with BE
  3. Reflux surgery not shown to prevent risk of cancer.
  4. Try and prevent progression from no dysplasia to HGD with endoscopic management
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45
Q

Describe the recommended endoscopic surveillance schedule for Barrett’s Esophagus?

A

**Endoscopic follow up BE **
- Australian Cancer Council Guidelines Barrett’s Oesophagus 2015
- DYSPLASIA Seattle criteria 4 quadrant biopsies every 2cms and careful endoscopic assessment of mucosa. Biopsy any mucosal abnormality.
- High grade dysplasia – need careful follow up and management as significant risk of adenocarcinoma
- Improve endoscopic assessment with new techniques-high definition endoscopy, chromoendoscopy, NBI, confocal microscopy – almost a histological image but not readily available. These techniques allow more targeted biopsies.

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46
Q

What are your options for Low and High grade Barrett’s Oesophagus? What is HALO?

A
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47
Q

How would you manage each of the following clinical scenarios?

A
  • Melissa = Lifestyle factors: reduce alcohol, weight loss, ant-acid, H2 blocker = MILD
  • Robert = Moderate = Gastroscopy – waking at night, cough could give aspiration, worried about Barretts, also age, overweight = PPI
  • Peggy = Weight gain = raised intradbominal pressure – pt had ascites = ovarian cancer
  • REMEMBER PRESSURE/MASS CAUSES
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48
Q

What is the epidemiology of Inflammatory Bowel Disease (IBD)?
- Peak age of diagnosis?
- Costs?

A
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49
Q

Aetiology of IBD?

A

Aetiology – not really known! But family hx important. Autoimmune?

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50
Q

Aetiology of IBD
- Smoking?
- OCP use?
- Appendectomy?

A
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51
Q

Effect of the microbiome of incidence of IBD?

A
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52
Q

How can you classify Ulcerative Colitis?
What is the Mayo Score for UC based on? (4)

A

UC - Classify by:
1. Disease extent: proctitis, left-sided disease, pancolitis
2. Severity
3. Colonic Mucosal Disease
4. Extraintestinal manifestations

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53
Q

What is Crohn’s Disease? Clinical Features?

A

Perianal disease much more common in Crohns vs. UC

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54
Q

How is the severity of Crohn’s disease scored?

A
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55
Q

What is the Montreal classification for Crohn disease?

A
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56
Q

List 6 symptoms of Crohn’s disease?

A
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57
Q

List 5 differential diagnoses of IBD?

A

Infections - C.Diff & UC – cytomegalovirus superimposed

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58
Q

List 11 investigations to consider in the diagnosis of IBD?

A

Faecal calprotectin = stool marker for inflammation. Elevated faecal calprotectin indicates the migration of neutrophils (produced by neutrophils) to the intestinal mucosa, which occurs during intestinal inflammation, including inflammation caused by inflammatory bowel disease.
- Faecal calprotectin is a very sensitive marker for inflammation in the gastrointestinal tract, and useful for the differentiation of inflammatory bowel disease (IBD) from irritable bowel syndrome (IBS).
- Not PBS subsidised in WA.

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59
Q

List 6 Extraintestinal manifestations of IBD?

A
  • Lots of cross over with rheumatology
  • Patients with IBD have an increased risk of DVT so should be put on VTE prophylaxis (eg. Clexane) if coming into hospital with an acute flare up.
  • Erythema Nodosum = round red raised nodules which are tender
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60
Q

List 3 Perianal diseases associated with IBD?

A

IBD - Perianal Disease
1. Skin tags
2. Abscesses
3. Fistulas

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61
Q

Discuss the broad treatment/management of IBD?

A
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62
Q

List 6 Drugs to consider in the medical management of IBD?

A

5ASA - Mesalazine, also known as mesalamine or 5-aminosalicylic acid = not as useful in crohns (full thickness) because it is only topical

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63
Q

Describe the role of steroids in the medical management of IBD?
- MOA: Local vs. Systemic?
- Side effects? (4)

A

Steroids = really limit!

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64
Q

List 3 Immunosuppressants you might consider in the medical management of IBD? What should you check for regularly with pts on these meds?

A

Must check drug metabolism enzyme level prior to commencing on azathioprine – pt might die

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65
Q

List 3 Biologicals you might consider in the medical management of IBD? What should you screen for before commencing a patient on these?

A
  • Infliximab
  • Vedolizumab mostly affective on the gut so if lots of extraintestinal manifestions, wont be very useful
  • Humira = one of the most expensive drugs on the PBS in Australia
  • High risk of infections on these drugs – need to screen prior to commencing – eg. Quantiferon Gold for TB
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66
Q

What are the surgical options for IBD?

A
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67
Q
A

Simplest drug to start with = Sulphasalazine or 5ASA drugs then Steroids – rectally - all ok during pregnancy.
Pt should be well before getting pregnant.

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68
Q

What is the Epidemiology of Coeliac disease?

A
  • Rare in Japan, China, southern India but high in north.
  • Correlates with wheat based diet and HLA typing in population
  • May increase with western-style diets replacing rice based diets. Historically seasonal diarrhoea related to crops.
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69
Q

What is the most important diagnostic test for Coeliac disease?

A

TTG = IgA antibodies so need to do that too because if your overall IgA is low its not accurate

70
Q

Describe the role of HLA Typing in Coeliac disease?

A

Need to have at least one of HLA DQ2 or DQ8 (genes) to have coeliac but it’s not diagnostics.

71
Q

What is the Gold Standard for the diagnosis of Coeliac Disease?

A

The patient cant be on a gluten-free diet at this stage or your biopsies and antibody levels wont be.

72
Q

Compare the histology of the normal small intestine with that of a patient with Coeliac disease?

A
73
Q

List 10 other causes of villous atrophy other than Coeliac disease?

A
  1. Crohns disease
  2. Eosinophilic gastroenteritis
  3. Giardiasis
  4. Lymphoma
  5. Post gastroenteritis
  6. Tropical sprue
  7. Zollinger- Ellison syndrome
  8. Autoimmune enteropathy
  9. Cows milk intolerance (children)
  10. Bacterial overgrowth
  11. Drugs : Olmesartan, Mycophenolate
74
Q

List 7 high risk groups or clinical presentations where you might consider screening for coeliac disease?

A
75
Q

What are 6 types/forms of coeliac disease?

A
76
Q

Describe the treatment for coeliac disease.

A
77
Q

List 3 risks associated with coeliac disease?

A
78
Q

What are your options for patient’s with coeliac disease who fail to respond to treatment.

A
79
Q

Describe the link between Coeliac disease and infertility?
When should you investigate?

A

**Coealic & Infertility **
* Estimates of prevalence in women with unexplained infertility 2 to 6 % (compared to current population 1%)
* Small studies and varying results
* 2010 Swedish study reported 11,495 women with CD and the number of children born. Overall same a general population but reduced in the 2 years preceding diagnosis.
* Results relate to mix of population.

80
Q

What is Non Coeliac Gluten Sensitivity (NCGS)?

A
81
Q

What is the FODMAPS diet?

A
82
Q

List 9 causes of acute surgical abdominal.

A
83
Q

Describe common causes of abdominal pain in the hospitalised patient.
- What could Right upper quadrant pain be caused by?
- Investigations?

A
84
Q

List 4 Biliary causes & their clinical features of right upper quadrant (RUQ) abdominal pain.

A
85
Q

List 5 Hepatic causes & their clinical features of right upper quadrant (RUQ) abdominal pain.

A
86
Q

List 8 Causes of epigastric abdominal pain and their associated clinical features?

A
87
Q

List 4 Causes of left upper quadrant (LUQ) abdominal pain and their associated clinical features?

A
88
Q

List 8 Causes of lower abdominal pain and their associated clinical features?

A
89
Q

What are 6 common causes for upper gastrointestinal blood loss?

A
90
Q

List 6 signs/symptoms of upper gastrointestinal blood loss?

A
91
Q

What are 7 common causes for lower gastrointestinal blood loss?

A
92
Q

List 6 symptoms of lower gastrointestinal blood loss?

A
93
Q

What is the role of contributing factors in GI bleeding? (List 8)

A
94
Q

What are 7 pathologic patterns of liver disease, their common causes and their pathologic features?

A
95
Q

List 7 Symptoms and Signs of IBD?

A
96
Q

List the Pathological Features of IBD - Crohns (4) and UC (4)?

A
97
Q

Describe the current investigation paradigms for inflammatory bowel disease.

A
98
Q

Describe the current management paradigms for inflammatory bowel disease.
- Medications (5)?
- Nutritional support?
- Surgical?
- Monitoring and follow-up?

A
99
Q

Describe the current investigation paradigms for peptic ulcer disease.

A
100
Q

Describe the current management paradigms for peptic ulcer disease.
- 4 Lifestyle Modifications?
- 3 Medications?
- Complication Management?
- Follow-up and Maintenance?

A
101
Q

What is the Incidence and Mortality of Colorectal Cancer?

A
102
Q

What are the 4 different types of colorectal polyps?

A
103
Q

What is the Adenoma Carcinoma Sequence?

A
  • The adenoma-carcinoma sequence is a concept that envisages the evolution of carcinoma of the colon and rectum by way of an intermediate benign entity, the adenoma.
  • The adenoma-carcinoma sequence (ACS) is defined by a set of recurrent driver mutations in APC, KRAS, SMAD4, and TP53 genes, that accumulate during adenoma formation and progression to sporadic colorectal cancer (CRC), often correlating with specific stages of the developmental process.
104
Q

Describe the Aetiology/Causes of CRC?
- List 6 high-risk genetic associations?

A

Majority = sporadic

105
Q

List 12 Factors increasing the risk of CRC?

A
106
Q

What are the relevant variables when assessing a family history of CRC?
- List 7 Red flags for the presence of a Hereditary CRC Syndrome?

A

CRC - Assessing Family History
- Number of relatives
- Age of CRC diagnosis
- Other cancers

107
Q

Who is considered to have an average or slightly above average risk of CRC? Management?

A
108
Q

Who is considered to have a moderate increased risk of CRC? Management?

A
109
Q

Who is considered to be high risk for CRC? Management?

A
110
Q

What is FAP? How is it linked to CRC?

A

Classic familial adenomatous polyposis, called FAP or classic FAP, is a genetic condition. It is diagnosed when a person develops more than 100 adenomatous colon polyps.

111
Q

What is Lynch Syndrome/HNPCC? How is it linked to CRC?

A

Lynch syndrome, also known as hereditary non-polyposis colorectal cancer (HNPCC), is the most common cause of hereditary colorectal (colon) cancer. People with Lynch syndrome are more likely to get colorectal cancer and other cancers, and at a younger age (before 50), including.

112
Q

How do we screen for CRC?

A
113
Q

Describe the procedure of a colonoscopy? 4 Risks?

A
114
Q

What percentage of lesions are missed during colonoscopy?

A
115
Q

What should you do with a patient after they have had a colonoscopy?

A
116
Q

List the 5 most common signs & symptoms of CRC?

A

Blood losing indications are the most significant.

117
Q

Describe the staging for CRC? (Duke vs. TNM)

A
118
Q

List 11 options for primary prevention of CRC?

A
119
Q

List 4 options for secondary prevention of CRC/polyps?

A
120
Q

Briefly describe the anatomy and histology of the liver?

A

Anatomy of the Liver
- Right and left lobe – separated by falciform ligament
- 8 segments
- 2 blood supplies: Hepatic artery & Portal vein.
- Hepatic artery – 20% of hepatic inflow, 50% of oxygen.
- Origin coeliac artery. Branches into right gastric artery, gastroduodenal and proper hepatic.
- Portal vein – 80% of hepatic inflow, 50% of oxygen
- Origin at the confluence of splenic and SMV. Branches to right and left portal vein

121
Q

What is Bilirubin?
Summarise Bilirubin metabolism.

A

Bilirubin
- End product of haemoglobin degradation
- Porphyrin portion of haemoglobin molecule is converted by macrophages into bilirubin and released into blood
- Unconjugated (insoluble) bilirubin is taken up by the liver and conjugated to be excreted in stool and urine
- In healthy individuals, majority of bilirubin should be unconjugated

122
Q

What are Alanine aminotransferase and aspartate aminotransferase?
- Which is specific to the liver?
- What can the ratio tell us?

A
  • ALT found predominantly in the liver in the cytosol of hepatocytes
  • AST less specific for liver disease, is a liver mitochondrial enzyme, and can be also found in cardiac/skeletal muscles, red blood cells and kidney
  • Damage to hepatocytes results in release of ALT and AST = “Hepatitic picture”
  • Ratio can be useful in alcoholic hepatitis or fibrosis – AST:ALT ratio of >2:1
  • Not useful as a prognostic factor – can have normal ALT/AST in chronic liver disease as not many hepatocytes left
123
Q

What is Alkaline Phosphatase?

A

ALP
- Present in liver cells and bile duct cells
- Raised in cholestasis or bile duct damage = “Obstructive picture” reflecting biliary obstruction
- Also produced in other parts of the body – bone, intestine, placenta
- Will see it in other diseases e.g. osteomalacia, Paget’s disease, bone mets
- Retained bile acids prompt increased production of ALP
- ALP also reduces secretory functions of biliary epithelium and promotes cholestatisis
- Needs to be interpreted in combination with GGT and bilirubin
- “Cholestatic” pattern

124
Q

What is Gamma glutamyl transferase?

A

GGT
- Located in the biliary pole of hepatocytes and bile duct cells
- Suggestive of cholestasis/obstruction or biliary epithelial damage
- Raised in response to alcohol and medications (phenytoin, warfarin, rifampicin)
- Raised in fatty liver disease
- Raised in biliary obstruction
- “Cholestatic picture”

125
Q

What is Albumin?
- Where is it synthesised?
- Function?
- When is it low?

A

Albumin
- Most abundant circulating protein in plasma
- Synthesized by hepatocytes and rapidly excreted into plasma
- Half life of 20 days
- Helps to maintain oncotic pressure and also acts as a transporter
- Low albumin can reflect liver disease but non specific
- May also be low in pregnancy, poor nutritional state, chronic inflammation, sepsis, renal disease
- Can be replaced but short lived

126
Q

What can a coagulation profile tell us about liver function?

A
  • Liver impairment can result in reduced production of clotting factor
  • Obstructive jaundice results in reduction of bile acids in intestine.
  • Reduced absorption of vitamin K which is essential for producing clotting factors II,VII, IX and X
  • Complex picture – an elevated coagulation test time (INR, APTT)
  • Acute disease – increased bleeding tendence due to reduced clotting factors
  • Chronic disease – increased thrombotic tendency due to reduced effects of thrombomodulin
127
Q

List 8 Functions of the liver?

A
128
Q

7 Causes of acute liver injury?

A
  1. Infective causes
  2. Drugs
  3. Vascular
  4. Autoimmune
  5. Malignancy
  6. Metabolic
  7. Pregnancy related
129
Q

Compare the different Hepatitis Viruses A-E.
What are 4 other viruses that can cause acute liver failure?

A

Other viruses that can cause Acute Liver Failure:
1. Herpes simplex virus
2. Ebstein barr virus
3. Cytomegalovirus
4. Parvovirus

130
Q

What are the two types of Drug induced liver injury? How can they present?

A
  • Predictable (dose dependent, well known) vs idiosyncractic (unpredictable)
  • Can present with a hepatitic or cholestatic injury
  • History is key to identifying timing of drug exposure
  • Drug discontinuation generally leads to improvement in liver injury (gradual)
  • 5-10% will develop chronic liver injury
  • Increasing number of herbal supplements causing liver injury – green tea extract, garcinia cambognia
131
Q
  • Discuss the impact of alcohol on the liver?
  • Risk of Cirrhosis?
  • Describe an approach to a patient with suspected alcohol liver disease?
A

Alcohol
- Excessive consumption can result in steatosis, alcoholic hepatitis and eventually cirrhosis.
- Alcohol is metabolised in the liver, resulting in formation of toxic acetaldehyde and free radicals.
- Characterised by jaundice within 60 days of heavy alcohol consumption for a minimum of 6 months, AST:ALT ratio of 2:1.
- Supportive treatment with cessation of alcohol use and thiamine
- Steroid therapy if Maddrey score >32.
- Lille score at 1 week to assess response. If adequate response, continue steroids for 28 days. If inadequate response, cease

132
Q

Metabolism of Paracetamol?

A

Paracetamol
- Accidental vs intentional
- Acute vs chronic
- Gastric decontamination no longer recommended
- Predisposing factors may increase risk of toxicity at lower dosages
- N-acetyl cysteine works by increasing hepatic gluthathione stores to allow more conjugation of NAPQI.
- Important to consider and address factors which led to overdose – psych review, webster pack for elderly patients with dementia.

133
Q

List 4 Ischaemic / Vascular causes of Acute Liver Injury?

A

Ischaemic / Vascular causes of Acute Liver Injury
1. Budd Chiari syndrome
2. Portal vein thrombosis
3. Hypotension secondary to shock/hypovolemia/ circulatory failure
4. Thrombotic state – pregnancy, OCP, polycythemia rubra vera

134
Q

List 3 Autoimmune Causes of Acute Liver Injury?
- Presentation?
- Diagnosis?
- Management?

A

Autoimmune causes of Acute Liver Injury
1. Autoimmune hepatitis
2. Primary biliary cholangitis
3. Primary sclerosing cholangitis

  • May be asymptomatic so can present late in the disease with cirrhosis
  • Diagnosed based on blood tests (ANA, AMA, anti-LKM, SMA), imaging (MRCP) and liver biopsy
  • Management with steroids/ursodeoxycholic acid
135
Q

Describe the malignant causes of acute liver injury.
- Prognosis?
- 3 Risk factors?
- Treatment?

A
  • Primary vs metastatic
  • Incidence of hepatocellular carcinoma is increasing = 7th most common cancer
  • Poor prognosis with 5 year survival of 20%
  • Risk factors: cirrhosis, hepatitis B, alcohol
  • Treated with surgery, locoregional therapies, immunotherapy, chemotherapy or transplant
136
Q

List 4 Metabolic Causes of Acute Liver Injury?

A

Metabolic Causes of Acute Liver Injury
1. Metabolic associated fatty liver disease
2. Haemochromatosis
3. Alpha 1 anti-trypsin: Autosomal dominant lung disease, Genetic testing and alpha 1 levels
4. Wilson’s disease: Neurologic symptoms, Family history, Kayser-Fleischer rings, Low caeruloplasmin and 24h urinary copper, Liver biopsy

137
Q

How can pregnancy cause acute liver injury?

A
138
Q

9 Symptoms of acute liver failure?

A

Symptoms of acute liver failure
1. Abdominal pain
2. Abdominal distention
3. Confusion
3. Jaundice
4. Dark urine
5. Pale stools
6. Pruritis
7. Bleeding
8. Anorexia

139
Q

9 Clinical features on physical examination of acute liver injury?

A
  1. Jaundice
  2. Scleral icterus
  3. Mental state and cognition
  4. Asterixis
  5. Ecchymoses or petechiae
  6. Hepatomegaly
  7. Ascites
  8. Pedal oedema
  9. Pleural effusion
140
Q

Describe the Management of acute liver failure? (11 points)
- What are the criteria for liver transplantation in acute liver failure?

A
  1. Treat underlying cause and prevent further insult if possible
  2. Transfer to a centre with ICU/transplant centre
  3. Monitor coagulation but do not correct if no acute bleeding (good prognostic value)
  4. Maintain normotension and normovolemia
  5. PPI prophylaxis for stress ulcer prevention
  6. Dialysis for renal failure
  7. Monitor for cerebral oedema
  8. Maintain nutrition
  9. Monitor for infection
  10. Correct metabolic abnormalities
  11. Consider transplant if not improving and meets criteria
141
Q

Describe a method for interpreting LFTs?
- 4 Patterns of Abnormality?

A

PATTERNS OF ABNORMALITY
1. Isolated GGT
2. Hepatitic – ALT or AST elevation
3. Cholestatic - bilirubin, ALP, GGT
4. Mixed

141
Q

List 13 investigations to order as part of a liver screen to identify the aetiology of hepatocellular injury?

A
  1. Hepatitis serology (A/B/C)
  2. Epstein-Barr Virus (EBV)
  3. Cytomegalovirus (CMV)
  4. Anti-mitochondrial antibody (AMA)
  5. Anti-smooth muscle antibody (ASMA)
  6. Anti-liver/kidney microsomal antibodies (Anti-LKM)
  7. Anti-nuclear antibody (ANA)
  8. p-ANCA
  9. Immunoglobulins – IgM/IgG
  10. Alpha-1 Antitrypsin (to rule out alpha-1 antitrypsin deficiency)
  11. Serum Copper (to rule out Wilson’s disease)
  12. Ceruloplasmin (to rule out Wilson’s disease)
  13. Ferritin (to rule out haemochromatosis)
142
Q
A
143
Q

Aetiology of Acute Li

A
144
Q

Describe the management of Acute Liver Injury:
- Stabilisation?
- Supportive measures?

A
145
Q

What is a MELD score?

A

Model for End-stage Liver Disease score:
A model used to predict mortality in patients with liver cirrhosis and to stratify patients awaiting liver transplantation. Takes into account renal function, bilirubin, INR, and plasma sodium.

146
Q

How does Chronic Liver Disease cause death?

A
  1. Portal hypertension due to cirrhosis
  2. Loss of function
  3. Liver cancer – hepatocellular carcinoma (85%) and cholangiocarcinoma (15%)
    - Cirrhosis (alcohol, viral hepatitis, fatty liver disease)
    - Noncirrhotic (fatty liver disease)
147
Q

What are the 2 ways in which the adult liver can regenerate?

A

LIVER REGENERATION - Two pathways by which adult liver can regenerate:
1. Hepatocyte mediated: mature hepatocytes divide to replenish lost liver mass - Acute injury (a.k.a Zeus)
2. Progenitor cell mediated: hepatocyte replicative arrest; adult liver progenitor cells proliferate, migrate and differentiate into mature hepatocytes and biliary epithelium = Chronic injury

148
Q

What is End Stage Liver Disease?
- Typical clinical manifestations?

A
149
Q

Describe an approach to suspected liver disease?
- What is the modified Child-Pugh Score?

A
150
Q

What is the commonest liver condition in Western world in children and adults?

A

NAFLD = Commonest liver condition in Western world in children and adults
NAFLD IN ADOLESCENTS WA DATA
◼ 15% of 16 yo have NAFLD (US Dx)
◼ More common in females
◼ 21% have other features of metabolic syndrome
◼ 60% of obese have NAFLD, 30% of overweight have NAFLD, 8% normal weight have NAFLD
◼ 80% of NAFLD have normal ALT

151
Q

What Environmental Factors are associated with NAFLD?

A

◼ NAFLD less common in children exclusively breast fed for at least 6 months
◼ More common in those who are obese and who consume increased fructose
◼ Female NAFLD more likely if maternal obesity and early – mid gestational weight gain > 6 kg
◼ Male NAFLD associated with lower family SES

152
Q

What is the treatment for NAFLD?

A
153
Q

What are the top 5 most commonly prescribed drugs in the Community?

A
  1. Augmentin 1 in 2350 patients (22%)
  2. Diclofenac 1 in 9480 patients (6%)
  3. Azathioprine 1 in 133 patients (4%)
  4. Infliximab 1 in 148 patients (4%)
  5. Nitrofurantoin 1 in 1369 patients (4%)
154
Q

How does Chronic Liver Disease cause Thrombocytopenia?

A
155
Q

Outline the Mechanisms of thrombocytopenia in liver cirrhosis?

A
156
Q

Name 2 tests which can be helpful when trying to work out if pre-hepatic hyperbilirubinaemia is caused by haemolysis?

A

Antiglobulin testing, also known as the Coombs test, is an immunology laboratory procedure used to detect the presence of antibodies against circulating red blood cells (RBCs) in the body, which then induce hemolysis.

157
Q

What are the 4 broad mechanisms of shock, their causes and pathophysiology?

A
158
Q

List 9 clinical symptoms and signs of shock?

A
159
Q

List 8 Symptoms and Signs of Pulmonary Embolism?

A
160
Q

List 11 Risk Factors for Pulmonary Embolism?

A
161
Q

List 8 Symptoms and Signs of Pneumothorax?

A

Pneumothorax refers to the presence of air in the pleural space, leading to lung collapse.

162
Q

List 7 Symptoms and Signs of Pneumothorax?

A

Pneumothorax refers to the presence of air in the pleural space, leading to lung collapse.

163
Q

List 6 major indications for intubation.

A

Intubation refers to the placement of a tube into the trachea to establish a secure airway and facilitate mechanical ventilation.

164
Q

What are 7 Clinical Signs of impending respiratory failure?

A

Impending respiratory failure refers to a critical condition in which a patient’s respiratory function is deteriorating, and there is an imminent risk of respiratory system failure.

165
Q

What are 7 Laboratory Signs of impending respiratory failure?

A
166
Q

List 10 Indications for transfer to higher care units (e.g. the intensive care unit)?

A

Transfer to higher care units, such as the intensive care unit (ICU), is typically considered when a patient’s condition requires a higher level of monitoring, specialized interventions, and multidisciplinary care.

167
Q

What is the general approach to the evaluation of ventricular tachycardia? (4 steps)

A

The evaluation and treatment of ventricular tachycardia (VT) involve a systematic approach to assess the patient’s hemodynamic stability, identify the underlying cause, and determine the appropriate management strategy.

168
Q

What is the general approach to the treatment of ventricular tachycardia? (4 options)

A
169
Q

What is the general approach to the evaluation and treatment of ventricular fibrillation? (7 steps)

A

The evaluation and treatment of ventricular fibrillation (VF) require prompt intervention due to its life-threatening nature. VF is characterized by disorganized and chaotic electrical activity in the ventricles, leading to a loss of effective cardiac contractions and cardiac output.

170
Q

Define hypertensive emergency and describe the signs and symptoms of 7 conditions associated with it.

A

Hypertensive emergency refers to a severe elevation in blood pressure (hypertension) that requires immediate medical intervention to prevent organ damage. It is a medical emergency that requires prompt evaluation and treatment to reduce blood pressure and protect vital organs from potential complications. Hypertensive emergency typically presents with significantly high blood pressure levels (systolic blood pressure >180 mmHg and/or diastolic blood pressure >120 mmHg) along with signs of acute end-organ damage.

171
Q

List 4 drugs used in the treatment of hypertensive emergencies?
- MOA?
- Route of administration?
- Dose?
- Time of Action?
- Uses?

A

YR3 - R1: General Medicine (8 decks)

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