Monday [23/5/22] Flashcards

(100 cards)

1
Q

What’s in a ReSPECAT conversation? [5]

A

ReSPECT conversations follow the ReSPECT process by:

  1. discussing and reaching a shared understanding of the person’s current state of health and how it may change in the foreseeable future,
  2. identifying the person’s preferences for and goals of care in the event of a future emergency,
  3. using that to record an agreed focus of care (either more towards life-sustaining treatments or more towards prioritising comfort over efforts to sustain life),
  4. making and recording shared decisions about specific types of care and realistic treatment that they would want considered, or that they would not want, and explaining sensitively advance decisions about treatments that clearly would not work in their situation,
  5. making and recording a shared decision about whether or not CPR is recommended.
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2
Q

How to verify a death [9]

A

To perform death confirmation:

  1. Wash your hands and don PPE if appropriate.
  2. Confirm the identity of the patient by checking their wrist band.
  3. Inspect for obvious signs of life such as movement and respiratory effort.
  4. Assess the patient’s response to verbal stimuli (e.g. “Hello, Mr Smith, can you hear me?”).
  5. Assess the patient’s response to pain using one of the following methods:

Apply pressure to the patient’s fingernail.
Perform a trapezius squeeze.
Apply supraorbital pressure.
6. Assess the patient’s pupillary reflexes using a pen torch: after death, the pupils become fixed and dilated.

  1. Palpate the carotid artery for a pulse: after death, this will be absent.
  2. Perform auscultation in an attempt to identify any heart or respiratory sounds:

Listen for heart sounds for at least 2 minutes.
Listen for respiratory sounds for at least 3 minutes.
The recommended amount of time to listen for heart and respiratory sounds can vary, but it is generally accepted that a minimum of five minutes of auscultation is required to establish that irreversible cardiorespiratory arrest has occurred. 1

  1. Wash your hands, dispose of PPE appropriately and exit the room, making sure the relevant doors and/or curtains are closed/drawn behind you
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3
Q

reasons to refer to the coroner for a death [10]

A

The cause of death is unknown.
The death was sudden or unexpected (inclusive of all deaths less than 24 hours after admission to hospital).
The deceased person had not seen a doctor within the 14 days before their death.
The death is considered suspicious, unnatural or violent.
The death may be due to an accident, self-neglect or neglect on the behalf of others.
The death is/could be due to the deceased’s prior employment (including industrial disease).
The death may be due to an abortion.
The death occurred during an operation or before recovery from anaesthetic.
The death occurred during or shortly after a period of police custody.
The death may be suicide

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4
Q

The 2 parts of the death certificate

A

Part 1 = cause of death [1a direct disease leading to death, 1b is the disease leading to 1a, 1c to 1b etc.]
Part 2 = conditions that may have contributed to the death

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5
Q

Families wish to get the patient cremated, what should you fill in?

A

Cremation form 4

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6
Q

Mrs June Morbid was an 87-year-old lady, whom you last attended to yesterday on the ward round with the consultant (Dr Spot). She had advanced Parkinson’s disease and was admitted 4 days previously with aspiration pneumonia. Unfortunately, the pneumonia did not respond to antibiotic treatment and the decision to palliate was made by the consultant after discussion with the family. Mrs Morbid peacefully passed away last night with her family around her, and her death was verified by your colleague on the night shift. You have been asked to fill in the death certificate after your ward round

A

1a] aspiration pneumonia

b] parkinsons disease

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7
Q

Mr Clive Matchstick (86-years-old) was admitted to the ward a week ago from a local nursing home having vomited and whilst in hospital, he developed urinary incontinence and sepsis. He was treated for urosepsis, under the care of Dr Johnson, but unfortunately, he passed away. You confirmed his death this morning and you had also reviewed him last night before going home. He has a past history of ischaemic heart disease, type 2 diabetes mellitus, Charcot’s deformity of the left foot and amputation of the big toe on the right foot

A

1a] urinary sepsis

2] IHD, T2Dm

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8
Q

Mr Samuel Clock (75-years-old) had been an in-patient on the ward you are working on for 2 weeks. He was being treated for community-acquired pneumonia (CURB-65 score of 4). His condition had progressively worsened when you reviewed him with his consultant Dr Tyvand last night and the decision was made to switch to a palliative approach of management. He passed away this morning, with his wife by his side. You confirmed his death on the ward. He has a past medical history of ischemic heart disease, hypertension, mesothelioma, type 2 diabetes and benign prostate hypertrophy

A

1a] CAP
b] pleural mesothelioma
2] IHD, T2DM

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9
Q

most common age acute appendicitis

A

10-20y/o

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10
Q

Pathogenesis of appendicitis [4]

A

lymphoid hyperplasia or a faecolith → obstruction of appendiceal lumen → gut organisms invading the appendix wall → oedema, ischaemia +/- perforation

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11
Q

Type of abdo pain seen in appendicitis [3]

A
  • peri-umbilical abdominal pain (visceral stretching of appendix lumen and appendix is midgut structure) radiating to the right iliac fossa (RIF) due to localised parietal peritoneal inflammation.
  • the migration of the pain from the centre to the RIF has been shown to be one of the strongest indicators of appendicitis
  • patients often report the pain being worse on coughing or going over speed bumps. Children typically can’t hop on the right leg due to the pain.
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12
Q

other features of appendicitis [4]

A
  • vomit once or twice but marked and persistent vomiting is unusual
  • diarrhoea is rare. However, pelvic appendicitis may cause localised rectal irritation of some loose stools. A pelvic abscess may also cause diarrhoea
  • mild pyrexia is common - temperature is usually 37.5-38oC. Higher temperatures are more typical of conditions like mesenteric adenitis
  • anorexia is very common. It is very unusual for patients with appendicitis to be hungry. Around 50% of patients have the typical symptoms of anorexia, peri-umbilical pain and nausea followed by more localised right lower quadrant pain
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13
Q

What is the Rovsing’s and psoas signs? [2]

A

Rovsing’s sign (palpation in the LIF causes pain in the RIF) is now thought to be of limited value
psoas sign: pain on extending hip if retrocaecal appendix

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14
Q

other general signs on examination of appendicits patient [3]

A

generalised peritonitis if perforation has occurred or localised peritonism
rebound and percussion tenderness, guarding and rigidity
retrocaecal appendicitis may have relatively few signs
digital rectal examination may reveal boggy sensation if pelvic abscess is present, or even right-sided tenderness with a pelvic appendix

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15
Q

Dx appendicitis [4]

A
  • raised inflammatory markers with history and examinations findings often enough to justify an appendicectomy
  • neutrophil-predominant leucoytosis seen in 80-90%
  • urine analysis to r/o pregnancy, renal colic and UTI
  • no definitive imaging techniques, often US if F
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16
Q

Mx of appendicitis 3[]

A

Appendicectomy [open or laparoscopic approach]
administration of prophylactic IV Abx
patients with perforated appendicitis [typically around 15-20%] require copious abdominal lavage

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17
Q

Research for just Abx with appendicitis [1]

A

trials have looked at the use of intravenous antibiotics alone in the treatment of appendicitis. The evidence currently suggests that whilst this is successful in the majority of patients, it is associated with a longer hospital stay and up to 20% of patients go on to have an appendicectomy within 12 months

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18
Q

Causes of ALF [4]

A
  • paracetamol
  • alcohol
  • viral hepatitis
  • AFL disease of pregnancy
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19
Q

Features of ALD [5]

A
jaundice
coagulopathy: raised prothrombin time
hypoalbuminaemia
hepatic encephalopathy
renal failure is common ('hepatorenal syndrome')
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20
Q

Most common causes of acute upper GI bleed [2]

A

Varicies or peptic ulcer

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21
Q

Clinical features of acute upper GI bleed [3]

A

haematemesis
the most common presenting feature
often bright red but may sometimes be described as ‘coffee gound’
melena
the passage of altered blood per rectum
typically black and ‘tarry’
a raised urea may be seen due to the ‘protein meal’ of the blood

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22
Q

Differentiate between varicies presentation and peptic ulcer disease presentation

A

oesophageal varices: stigmata of chronic liver disease

peptic ulcer disease: abdominal pain

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23
Q

Usually a large volume of fresh blood. Swallowed blood may cause melena. Often associated with haemodynamic compromise. May stop spontaneously but re-bleeds are common until appropriately managed

A

oesophageal varicies

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24
Q

Usually small volume of blood, except as a preterminal event with erosion of major vessels. Often associated symptoms of dysphagia and constitutional symptoms such as weight loss. May be recurrent until managed

A

cancer

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25
Small volume of fresh blood, often streaking vomit. Malena rare. Often ceases spontaneously. Usually history of antecedent GORD type symptoms
oesophagitis
26
Typically brisk small to moderate volume of bright red blood following a bout of repeated vomiting. Malena rare. Usually ceases spontaneously
mallory weiss tear
27
Small low volume bleeds are more common so would tend to present as iron deficiency anaemia. Erosion into a significant vessel may produce considerable haemorrhage and haematemesis.
gastric ulcer
28
May be frank haematemesis or altered blood mixed with vomit. Usually prodromal features of dyspepsia and may have constitutional symptoms. Amount of bleeding variable but erosion of major vessel may produce considerable haemorrhage
gastric Ca
29
Usually haematemesis and epigastric discomfort. Usually there is an underlying cause such as recent NSAID usage. Large volume haemorrhage may occur with considerable haemodynamic compromise
Diffuse erosive gastritis
30
Often no prodromal features prior to haematemesis and melena, but this arteriovenous malformation may produce quite a considerable haemorrhage and may be difficult to detect endoscopically
Dieulafoy lesion
31
Features of a duodenal ulcer [4]
These are usually posteriorly sited and may erode the gastroduodenal artery. However, ulcers at any site in the duodenum may present with haematemesis, melena and epigastric discomfort. The pain of a duodenal ulcer is slightly different to that of gastric ulcers and often occurs several hours after eating. Periampullary tumours may bleed but these are rare
32
Which artery is affected commonly in duodenal ulcer? [1]
gastroduodenal artery
33
In patients with previous abdominal aortic aneurysm surgery aorto-enteric fistulation remains a rare but important cause of major haemorrhage associated with high mortality
Aortic-enteric fistula
34
List causes of upper Gi bleed []
Oesophageal causes - varicies - oesophagitis - cancer - mallory weiss tear gastric causes - ulcer - cancer - dieulafoy lesion - diffuse erosive gastritis duodenal causes - ulcer - aorto-enteric fistula
35
Ways of risk assessing an upper GI bleed [2]
the Glasgow-Blatchford score at first assessment - helps clinicians decide whether patient patients can be managed as outpatients or not the Rockall score is used after endoscopy - provides a percentage risk of rebleeding and mortality - includes age, features of shock, co-morbidities, aetiology of bleeding and endoscopic stigmata of recent haemorrhage
36
What does high urea levels mean for Gi bleeds?
It's an upper Gi bleed due to the protein meal
37
Which patients with an acute upper GI bleed may be considered for early discahrge
Blathcford score of 0
38
First steps for acute upper Gi bleed [4]
ABC, wide-bore intravenous access * 2 platelet transfusion if actively bleeding platelet count of less than 50 x 10*9/litre fresh frozen plasma to patients who have either a fibrinogen level of less than 1 g/litre, or a prothrombin time (international normalised ratio) or activated partial thromboplastin time greater than 1.5 times normal prothrombin complex concentrate to patients who are taking warfarin and actively bleeding
39
What should be offered within 24h of an upper GI bleed [2]
should be offered immediately after resuscitation in patients with a severe bleed all patients should have endoscopy within 24 hours
40
Mx of non-variceal bleeding [2]
NICE do not recommend the use of proton pump inhibitors (PPIs) before endoscopy to patients with suspected non-variceal upper gastrointestinal bleeding although PPIs should be given to patients with non-variceal upper gastrointestinal bleeding and stigmata of recent haemorrhage shown at endoscopy if further bleeding then options include repeat endoscopy, interventional radiology and surgery
41
Mx of variceal bleeding [3]
terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e. before endoscopy) band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures
42
Alcohol limit per week adults [2]
Men and women should drink no more than 14 units per week. | If you're doing it, it should be spred over 3d.
43
Pregnancy and alcohol [1]
pregnant women should not drink. The wording of the official advice is 'If you are pregnant or planning a pregnancy, the safest approach is not to drink alcohol at all, to keep risks to your baby to a minimum. Drinking in pregnancy can lead to long-term harm to the baby, with the more you drink the greater the risk
44
Define one unit of alcohol
10mL of pure ethanol
45
Calculate the units ofone pint of 5% beer or lager [1]
568 * 5 / 1000 = 2.8 units
46
How does alcoholic ketoacidosis typically present? [4]
Metabolic acidosis Elevated anion gap Elevated serum ketone levels Normal or low glucose concentration
47
Tx for alcoholic ketacidosis [2]
The most appropriate treatment is an infusion of saline & thiamine. Thiamine is required to avoid Wernicke encephalopathy or Korsakoff psychosis
48
What does ALD cover? [3]
alcoholic fatty liver disease, alcoholic hepatitis, cirrhosis
49
Selected investigation findings for ALD [2]
gamma-GT is characteristically elevated | the ratio of AST:ALT is normally > 2, a ratio of > 3 is strongly suggestive of acute alcoholic hepatitis
50
What AST:ALT ratio is strongly suggestive of acute alcoholic hepatitis
ratio of over 3
51
Main Mx of alcoohlic hepatitis
glucocorticoids (e.g. prednisolone) are often used during acute episodes of alcoholic hepatitis
52
What's used during acute episodes to determine who would benefit from glucocorticoid therapy? [2]
Maddrey's discriminant function (DF) is often used during acute episodes to determine who would benefit from glucocorticoid therapy it is calculated by a formula using prothrombin time and bilirubin concentration
53
What other drug is commonly used? [1]
Pentoxyphylline - the STOPAH study (see reference) compared the two common treatments for alcoholic hepatitis, pentoxyphylline and prednisolone. It showed that prednisolone improved survival at 28 days and that pentoxyphylline did not improve outcomes
54
Examples aminosalicylate drugs [3]
Sulphasalazine, mesalazine, olsalazine
55
What are aminosalicyclic acid drugs also known as? How do they work? [2]
5-aminosalicyclic acid (5-ASA) is released in the colon and is not absorbed. It acts locally as an anti-inflammatory. The mechanism of action is not fully understood but 5-ASA may inhibit prostaglandin synthesis
56
What is sulphalsazine? [2]
a combination of sulphapyridine (a sulphonamide) and 5-ASA
57
SE of sulhpapayridine[2]
many side-effects are due to the sulphapyridine moiety: rashes, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, lung fibrosis
58
benefit of taking mesalazine [2]
a delayed release form of 5-ASA | sulphapyridine side-effects seen in patients taking sulphasalazine are avoided
59
Se of mesalazine [3]
mesalazine is still however associated with side-effects such as GI upset, headache, agranulocytosis, pancreatitis*, interstitial nephritis
60
What is olsalazine/ [1]
two molecules of 5-ASA linked by a diazo bond, which is broken by colonic bacteria
61
What and why is a key Ix for patients taking aminosalicyclate drugs [2]
Aminosalicylates are associated with a variety of haematological adverse effects, including agranulocytosis - FBC is a key investigation in an unwell patient taking them.
62
What is way more common in patients takin mesalazine than sulfasalzine [1]
*pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine
63
What is angiodyslplasia? [2]
Angiodysplasia is a vascular deformity of the gastrointestinal tract which predisposes to bleeding and iron deficiency anaemia. There is thought to be an association with aortic stenosis, although this is debated. Angiodysplasia is generally seen in elderly patients
64
Dx and Mx of angiodysplasia [2]
Diagnosis - colonoscopy - mesenteric angiography if acutely bleeding Management - endoscopic cautery or argon plasma coagulation - antifibrinolytics e.g. Tranexamic acid - oestrogens may also be used
65
Antidiarrhoeal agents [2]
loperamide | diphenoxylate
66
What is SBP? [2]
Spontaneous bacterial peritonitis (SBP) is a form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis.
67
Features or SBP [3]
ascites abdominal pain fever
68
Dx of SBP [2]
paracentesis: neutrophil count > 250 cells/ul | the most common organism found on ascitic fluid culture is E. coli
69
Mx of SBP [1]
intravenous cefotaxime is usually given
70
When should Abx be given to patients with SBP? [3]
- patients who have had an episode of SBP - patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome - NICE recommend: 'Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved'
71
What is a marker for poor prognsosi with SBP? [1]
Alcoholic liver disease
72
What is ascites? [1]
Collection of abnormal fluid in the abdomen
73
What does SAAG over 11g/l indicate? [4]
SAAG > 11g/L (indicates portal hypertension) SAAG <11g/L Liver disorders are the most common cause - cirrhosis/alcoholic liver disease - acute liver failure - liver metastases Cardiac - right heart failure - constrictive pericarditis Other causes - Budd-Chiari syndrome - portal vein thrombosis - veno-occlusive disease - myxoedema
74
What does SAAG below 11g/l indicate? [4]
Hypoalbuminaemia nephrotic syndrome severe malnutrition (e.g. Kwashiorkor) Malignancy peritoneal carcinomatosis Infections tuberculous peritonitis ``` Other causes pancreatitisis bowel obstruction biliary ascites postoperative lymphatic leak serositis in connective tissue diseases ```
75
Mx of ascites [6]
1. Reduce dietary sodium 2. Fluid restriction if sodium below 125mmol/l 3. Aldosterone antagonist e.g. spirinolactone [also osmetimes loop diuretics 4. drianage if tense ascites 5. prophylactic Abx to reduce risk of SBP 6. TIPS may be considered in some patietns
76
How is tense ascites managed? [2]
large-volume paracentesis for the treatment of ascites requires albumin 'cover'. Evidence suggests this reduces paracentesis-induced circulatory dysfunction and mortality paracentesis induced circulatory dysfunction can occur due to large volume paracentesis (> 5 litres). It is associated with a high rate of ascites recurrence, development of hepatorenal syndrome, dilutional hyponatraemia, and high mortality rate
77
Recognised assocations of autoimmune hepatitis [3]
Autoimmune hepatitis is condition of unknown aetiology which is most commonly seen in young females. Recognised associations include other autoimmune disorders, hypergammaglobulinaemia and HLA B8, DR3. Three types of autoimmune hepatitis have been characterised according to the types of circulating antibodies present
78
Type 1 autoimmune hepatitis
Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA) Affects both adults and children
79
Type 2 autoimmune hepatitis
Anti-liver/kidney microsomal type 1 antibodies (LKM1) Affects children only
80
Type 3 autoimmune hepatitis
Soluble liver-kidney antigen Affects adults in middle-age
81
Features of autoimmune hepatitis
may present with signs of chronic liver disease acute hepatitis: fever, jaundice etc (only 25% present in this way) amenorrhoea (common) ANA/SMA/LKM1 antibodies, raised IgG levels liver biopsy: inflammation extending beyond limiting plate 'piecemeal necrosis', bridging necrosis
82
Mx of autoimmune hepatitis
steroids, other immunosuppressants e.g. azathioprine | liver transplantation
83
What is Barrett's oesophagus? [2]
Barrett's refers to the metaplasia of the lower oesophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium.
84
What does Barrett's increase the risk of? [1]
There is an increased risk of oesophageal adenocarcinoma, estimated at 50-100 fold
85
Screening Barrett's [1]
There are no screening programs for Barrett's - it's typically identified when patients have an endoscopy for evaluation of upper gastrointestinal symptoms such as dyspepsia.
86
Subdivision of Barrett'a oesophagus [2]
Barrett's can be subdivided into short (<3cm) and long (>3cm). The length of the affected segment correlates strongly with the chances of identifying metaplasia.
87
How common is Barrett's? [1]
The overall prevalence of Barrett's oesophagus is difficult to determine but may be in the region of 1 in 20 and is identified in up to 12% of those undergoing endoscopy for reflux. FUCKKKK
88
RFs of Barrett's
gastro-oesophageal reflux disease (GORD) is the single strongest risk factor male gender (7:1 ratio) smoking central obesity
89
Is alcohol a RF for Barrett's? [1]
Interestingly alcohol does not seem to be an independent risk factor for Barrett's although it is associated with both GORD and oesophageal cancer.
90
Mx of Barrett's [2]
endoscopic surveillance with biopsies high-dose proton pump inhibitor: whilst this is commonly used in patients with Barrett's the evidence base that this reduces the change of progression to dysplasia or induces regression of the lesion is limited
91
How often should endoscopic surveillance be carried out with Barrett's?
for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years
92
Intervention option for Barrett's [2]
endoscopic mucosal resection | radiofrequency ablation
93
What can bile-acid malsoprtion cause?
Bile-acid malabsorption is a cause of chronic diarrhoea. This may be primary, due to excessive production of bile acid, or secondary to an underlying gastrointestinal disorder causing reduced bile acid absorption. It can lead to steatorrhoea and vitamin A, D, E, K malabsorption.
94
Causes of bile-acid malabsorption [3]
Secondary causes are often seen in patients with ileal disease, such as with Crohn's. Other secondary causes include: cholecystectomy coeliac disease small intestinal bacterial overgrowth
95
Which test is done for bile-acid malabsorption? [3]
the test of choice is SeHCAT nuclear medicine test using a gamma-emitting selenium molecule in selenium homocholic acid taurine or tauroselcholic acid (SeHCAT) scans are done 7 days apart to assess the retention/loss of radiolabelled 75SeHCAT
96
Mx of bile-acid malabsorption
bile acid sequestrants e.g. cholestyramine
97
What is bilirubin a breakdown of? [1]
Heme, from RBCs
98
What do raised levels of unconjugated bilirubin suggest? [2]
Raised levels of unconjugated bilirubin may occur as a result of haemolysis, which is to say a pre-hepatic source, for example, autoimmune-mediated haemolytic anaemia. Red blood cell breakdown exposes heme-containing proteins and, as discussed above, these are then processed to form unconjugated bilirubin Hepatocyte defects, such as a compromised hepatocyte uptake of unconjugated bilirubin and/or defective conjugation may occur in liver disease, or deficiency of glucuronyl transferase. A mild glucuronyl transferase deficiency results in Gilbert's Syndrome, whilst a moderate to severe glucuronyl transferase deficiency may be seen in Crigler-Najjar Syndrome types I and II respectively. A transient glucuronyl transferase deficiency may also contribute to physiological neonatal jaundice.
99
What do raised levels of conjugated bilirubin suggest? [2]
Raised levels of conjugated bilirubin can result from defective excretion of bilirubin, for example, Dubin-Johnson Syndrome, or cholestasis.
100
When does jaundice start to appear? []1
Bilirubin in excess of 35umol/l