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Yr 5 - A&E > Revision > Flashcards

Revision Flashcards

1
Q

How is paracetamol metabolised?

A

1) 95% undergoes glucuronidation (with glutathione) –> creates water-soluble paracetamol conjugate that is eliminated in urine

2) 5% is metabolised by P450 enzymes –> into toxic NAPQI metabolite

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2
Q

What is the toxic metabolite of paracetamol?

A

NAPQI

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3
Q

How is the toxic NAPQI excreted?

A

1) NAPQI binds to glutathione

2) Becomes a non-toxic metabolite that is excreted in urine

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4
Q

A deficiency in what can predipose to paracetamol OD?

A

Glutathione deficiency e.g. eating disorders, alcohol use

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5
Q

How can acetylcysteine affect lab tests in paracetamol overdose?

A

Some lab analysers may underestimate paracetamol conc by as much as 40% if the blood test is taken during treatment with acetylcysteine.

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6
Q

What is plasma paracetamol conc that indicates treatment at 4 hours after ingestion?

A

100 mg/litre

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7
Q

What is plasma paracetamol conc that indicates treatment at 8 hours after ingestion?

A

50 mg/litre

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8
Q

In patients who present 8-24 hours after ingestion of an acute overdose, what amount of paracetamol ingested indicates the need for immediate acetylcysteine?

A

> 150 mg/kg

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9
Q

In patients who present >24 hours after ingestion of an acute overdose, what would indicate the need to start acetylcysteine?

A

1) ingested >150 mg/kg

2) jaundice

3) hepatic tenderness

4) raised ALT

5) INR >1.3

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10
Q

How is acetylcysteine given in paracetamol overdose?

A

IV infusion over 1 hour

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11
Q

When is acetylcysteine most effective in paracetamol overdose?

A

Within 8 hours of paracetamol ingestion

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12
Q

How can excessive dosage of acetylcysteine be avoided in obese patients?

A

Use a ceiling weight of 110kg

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13
Q

Main adverse effect of IV acetylcysteine?

A

Commonly causes an anaphylactoid reaction (non-IgE mediated mast cell release.

Stop the infusion and restart at a slower rate.

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14
Q

Criteria for liver transplant following paracetamol overdose (i.e. paracetamol liver failure)?

A

1) Arterial pH <7.3 24h after ingestion

or all of the following:
2) prothrombin time > 100 seconds
3) creatinine > 300 µmol/l
4) grade III or IV encephalopathy

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15
Q

What criteria is used to identify which patients with fulminant hepatic failure should be referred for liver transplantation?

A

Kings College Criteria (KCC)

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16
Q

Give 2 examples of drugs that can be used in chronic withdrawal of alcohol (i.e. preventing relapse)?

A

1) Disulfram

2) Acamprosate

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17
Q

Role of disulfram in alcohol mx?

A

Inhibits acetaldehyde dehydrogenase.

Drinking alcohol then causes severe reaction e.g. vomiting

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18
Q

Contraindications for disulfram? (2)

A

1) IHD

2) Psychosis

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19
Q

Mechanism of acamprosate in alcohol mx?

A

‘Anti craving’

Weak antagonist of NMDA glutamate receptors

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20
Q

Pathophysiology of alcoholic ketoacidosis?

A

1) Often alcoholics will not eat regularly and may vomit food that they do eat, leading to episodes of starvation.

2) Once the person becomes malnourished, after an alcohol binge the body can start to break down body fat, producing ketones.

3) Hence the patient develops a ketoacidosis.

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21
Q

Blood glucose level in alcoholic ketoacidosis?

A

Normal (or low)

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22
Q

Management of alcoholic ketoacidosis?

A

Saline & thiamine

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23
Q

How does ataxia in Wernicke’s typically present?

A

Truncal ataxia

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24
Q

What scale can be used to assess alcohol withdrawal severity?

A

Clinical Institute Withdrawal Assessment (CIWA-Ar)

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25
Q

What is the single most important prognostic factor following paracetamol OD?

A

Arterial pH

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26
Q

Where is McBurney’s point?

A

1/3 distance from ASIS to the umbilicus.

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27
Q

What does rebound tenderness & percussion tenderness indicate?

A

Ruptured appendix

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28
Q

What is psoas sign?

A

Pain on extending hip (if retrocaecal appendix)

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29
Q

When a patient has a clinical presentation suggestive of appendicitis, but investigations are negative, what is the next investigation?

A

Perform a diagnostic laparoscopy: to visualise the appendix directly.

30
Q

What does mesenteric adenitis typically follow?

A

Viral URTI or tonsillitis

31
Q

Which condition is clinically indistinguishable from appendicitis and is often identified when a normal appendix is found during laparoscopic appendicectomy?

A

Meckel’s diverticulum

32
Q

Cause of hypovolaemia in SBO?

A

1) GI tract secretes fluid that is later absorbed in colon

2) When there is an obstruction, and fluid cannot reach the colon, it cannot be reabsorbed

3) As a result, there is fluid loss from the intravascular space into the GI tract –> hypovolaemia & shock

33
Q

How does location of SBO affect fluid loss?

A

The higher up the intestine the obstruction, the greater the fluid losses as there is less bowel over which the fluid can be reabsorbed.

34
Q

What is the most common cause of SBO?

A

Adhesions

35
Q

Most common causes of SBO in adults?

Mneumonic: HANG IVs

A

H - hernias (2nd most common)
A - adhesions (most common)
N - neoplasm
G - gallstone ileus

I - intussusception
V - volvulus
s - strictures e.g. Crohn’s

36
Q

Does abdo pain come before or after vomiting in SBO?

A

Before (constant pain may indicate bowel ischaemia)

37
Q

What are the main causes of intestinal adhesions?

A

1) Abdominal or pelvic surgery (particularly open surgery)

2) Peritonitis

3) Endometriosis

4) Abdominal or pelvic infections (e.g. PID)

38
Q

Management of closed loop bowel obstruction?

A

Emergency surgery

39
Q

1st line investigation in SBO?

A

AXR

40
Q

What diameter indicates dilated small bowel loops?

A

> 3cm

41
Q

What are the upper limits of the normal diameter of the bowel?

A

3 cm: small bowel
6 cm: colon
9 cm: caecum

42
Q

What are valvulae conniventes?

A

Mucosal folds that form lines extending the FULL width of the bowel that are present in the small bowel.

These are seen on an abdominal x-ray as lines across the ENTIRE width of the bowel.

43
Q

What are haustra?

A

Haustra are like pouches formed by the muscles in the walls of the large bowel.

They form lines that do NOT extend the full width of the bowel.

These are seen on an AXR as lines that extend only part of the way across the bowel.

44
Q

What complications of SBO would require an ABCDE approach?

A

1) Perforated bowel

2) Bowel ischaemia

3) Hypovolaemic shock

4) Sepsis

45
Q

Non-operative mx of SBO?

A

Conservative:

1) NG tube

2) NBM

3) IV fluids & electrolytes

4) Observation

46
Q

Complications of SBO?

A

1) Bowel ischaemia

2) Sepsis

3) Short bowel syndrome

47
Q

What may indicate bowel ischaemia in SBO?

A

A change in the character of the pain (e.g. intermittent to continuous pain, increase in severity) or worsening of abdominal signs (e.g. rebound tenderness, guarding)

48
Q

Complications of short bowel syndrome?

A

With reduction in the surface area and distance for absorption of gastric nutrients, it essentially may lead a patient to require lifelong supplemental nutrition or intestinal transplantation.

49
Q

What is the main cause of LBO?

A

Cancer

50
Q

LBO is the initial presenting complaint of colonic malignancy in approximately 30% of cases.

What location of tumours if this more common in? Why?

A

This is particularly the case in more DISTAL colonic and rectal tumours, as these tend to obstruct earlier due to the SMALLER lumen diameter.

51
Q

What is the most common site of malignancy causing LBO?

A

Rectosigmoid (70%)

52
Q

What is the most common BENIGN cause of LBO?

A

Volvulus - when a loop of intestine twists around itself and the mesentery that supplies it, causing a bowel obstruction.

53
Q

Volvulus of what part of the colon is most common causing LBO?

A

Sigmoid colon

54
Q

Where does diverticular disease normally occur?

A

Sigmoid colon

55
Q

How does LBO affect potassium?

A

Hyperkalaemia due to release of intracellular K+

56
Q

Describe abdo pain in SBO vs LBO

A

SBO - colicky & intermittent

LBO - constant

Note - Sudden relief of pain followed by progressive worsening may suggest perforation

57
Q

What investigation is useful to differentiate between a mechanical LBO and a pseudo-obstruction?

A

Contrast enema

58
Q

Who is a contrast enema contraindicated in?

A

In cases of perforation due to leakage of contrast into the abdominal cavity and subsequent irritation.

59
Q

3 key differentials for a LBO?

A

1) SBO

2) Paralytic ileus

3) Toxic megacolon

60
Q

In 15% of cases, why may a LBO present with features more classical of a SBO?

A

As 15% of people have an incompetent ileo-caecal valve, therefore this will decompress the large bowel into the distal small bowel, therefore resembling a distal SBO instead.

61
Q

What is a pseudo-obstruction typically caused by?

A

Impairment of autonomic nervous system (functional obstruction)

Often a history of severe illness, injury or surgery e.g. severe chest infection, orthopaedic trauma, electrolyte imbalance

62
Q

What is toxic megacolon often associated with?

A

C. diff infection (likely Abx use)

63
Q

1st line mx of sigmoid volvulus?

A

Endoscopic decompression

64
Q

What is the definitive diagnostic investigation for SBO?

A

Abdo CT

65
Q

Can serum amylase be raised in SBO?

A

Yes

66
Q

What is given prior to an appendicectomy?

A

Prophylactic IV Abx

67
Q

What is the commonest cause of liver failure in the UK?

A

Paracetamol OD

68
Q

What is fetor hepaticus?

A

Sweet and fecal breath –> sign of liver failure (late sign of hepatic encephalopathy)

69
Q

Loin to groin pain + shock?

A

Think AAA

70
Q
A

Yr 5 - A&E (8 decks)

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