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Finals > Hepatobiliary > Flashcards

Hepatobiliary Flashcards

1
Q

Where is appendicitis pain?

A

Central then moves to the right iliac fossa

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2
Q

Where is the appendix?

A

Arises from the caecum with a single opening that connects it to the bowel

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3
Q

Where do the pathogens in appendicitis get trapped?

A

Get trapped due to obstruction at the point where the appendix meets bowel

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4
Q

What are the clinical signs in appendicitis?

A
  1. Tenderness at McBurney’s point (1/3 from ASIS to umbilicus)
  2. Rovsing’s sign: palpation in LIF causes pain in RIF
  3. Guarding
  4. Rebound tenderness in RIF: increased pain when suddenly releasing the pressure of deep palpation
  5. Percussion tenderness
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5
Q

What is the diagnostic test for appendicitis?

A

CT
If clinical presentation +ve but investigations -ve then diagnostic laparoscopy +/- appendicectomy

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6
Q

How does bowel obstruction cause hypovolaemia?

A

The GI tract secretes fluid that is later absorbed in the colon but in obstruction fluid cannot reach the colon and so cannot be reabsorbed. There is fluid loss from the intravascular space into the GI tract so hypovolaemia and shock (third spacing). The higher up the obstruction, the greater the fluid losses

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7
Q

What are the causes for small bowel obstruction?

A

Adhesions (surgery, peritonitis, infections, endometriosis, congenital, radiotherapy)
Hernias
Diverticular disease

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8
Q

What are the causes for large bowel obstruction?

A

Malignancy
Volvulus
Diverticular disease

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9
Q

What are the upper limits of bowel diameter?

A

Small bowel: 3cm
Colon: 6cm
Caecum: 9cm

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10
Q

How do you differentiate small bowel from large bowel on an X-ray?

A

Small bowel has valvulae conniventes (mucosal folds) which are seen across the full width of small bowel.
Large bowel has haustra (pouches formed by muscle) and they do not extend the full width of the bowel.

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11
Q

What is shown on VBG/ABG in bowel obstruction?

A

Metabolic alkalosis

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12
Q

What is the first line investigation in bowel obstruction?

A

Abdominal X-ray

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13
Q

What is the diagnostic investigation for bowel obstruction?

A

Contrast abdominal CT

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14
Q

What is the management of bowel obstruction?

A

Initial: drip and suck (nil by mouth, IV fluids, NG tube)
Definitive: surgery.

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15
Q

Which part of the bowel does ileus affect?

A

Small bowel

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16
Q

What causes ileus?

A

Injury to bowel
Handling during surgery
Inflammation/infection
Electrolyte disturbance: hypokalaemia, hyponatraemia

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17
Q

How does ileus present?

A

Same as bowel obstruction

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18
Q

How do you differentiate between ileus and bowel obstruction?

A

Ileus has absent bowel sounds whereas bowel obstruction has tinkling in early.

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19
Q

What is the management of ileus?

A

Nil by mouth
NG tube if vomiting
IV fluids
TPN if required.

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20
Q

What are the main types of volvulus?

A

Sigmoid (most common) and caecal (tends to affect younger patients)

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21
Q

What is a key cause of sigmoid volvulus?

A

Chronic constipation (colon becomes overloaded with faeces, sinks downwards causing a twist)

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22
Q

What is a volvulus?

A

The bowel wraps around itself and the mesentery it is attached to

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23
Q

What are risk factors for volvulus?

A

Neuropsychiatric disorders e.g. PD, schizophrenia, Duchenne muscular dystrophy
Chronic constipation
High fibre diet
Pregnancy
Adhesions

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24
Q

How does volvulus present

A

Same as bowel obstruction

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25
Q

How does bowel obstruction present?

A

Green bilious vomiting
Abdominal distension
Diffuse pain
Absolute constipation and lack of flatulence

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26
Q

What is shown on X-ray in volvulus?

A

“Coffee bean sign” in sigmoid
Small bowel obstruction in caecal

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27
Q

What is the diagnostic investigation for volvulus?

A

Contrast abdominal CT

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28
Q

What is the management of volvulus?

A

Initial: nil by mouth, NG tube, IV fluids
Conservative if sigmoid without peritonitis: decompression via rigid sigmoidoscopy and flatus tube insertion
Definitive: Hartmann’s (removal of rectosigmoid colon and formation of colostomy) in sigmoid volvulus
Ileocaecal resection/right hemicolectomy for caecal volvulus.

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29
Q

What are the complications of an incarcerated hernia?

A

Incarceration: hernia is irreducible so bowel is trapped in the herniated position and cannot be pushed back in
Obstruction: blockage of passage of faeces in bowel
Strangulation: when the hernia is non-reducible and the base becomes so tight that it cuts off blood supply, causing ischaemia

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30
Q

What are the surgical options for hernia repair?

A

Tension free repair: place mesh over the defect and suture to muscles/tissues either side. Decreased recurrent rate but may be complications with the mesh
Tension repair: suture the muscle/tissue on either side back together. Now rarely performed. Can cause pain

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31
Q

How does an indirect inguinal hernia form?

A

During fetal development, the processes vaginalis allows the testes to descend from the abdominal cavity through the inguinal canal and into the scrotum. If this remains intact, bowel can herniate through the inguinal canal and into the scrotum

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32
Q

What is the location of inguinal hernias?

A

Superior and medial to the pubic tubercle

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33
Q

How does a direct inguinal hernia form?

A

Protrudes directly through the abdominal wall, through Hesselbach’s triangle

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34
Q

How do you differentiate between a direct and indirect inguinal hernia?

A

Apply pressure with two fingers to the deep inguinal ring (midway from ASIS to the pubic tubercle). An indirect hernia will remain reduced

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35
Q

What is the anatomical location of the deep inguinal ring?

A

Where the inguinal ring connects to the peritoneal cavity.
The superficial inguinal ring is where the inguinal ring connects to the scrotum.

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36
Q

What is the location of femoral hernias?

A

Inferior and lateral to pubic tubercle.

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37
Q

Why are femoral hernias at high risk of obstruction and strangulation?

A

Femoral ring (opening between femoral canal and peritoneal cavity) is only very narrow

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38
Q

What is the management of a femoral hernia?

A

Urgent surgical repair within 2 weeks

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39
Q

What are other types of hernia?

A

Incisional hernia (often wide neck so left alone)
Umbilical hernia (common in newborns)
Epigastric hernia
Spieglian hernia (occur between lateral border of rectus abdominis and the linear semilunaris). USS to diagnose. Generally narrow base so high risk of complications
Diastasis recti (larger gap between rectus muscles)
Obturator hernia (abdominal/pelvic contents herniate through the obturator foramen at the bottom of the pelvis due to defect in the pelvic floor). May present with irritation to obturator nerve (pain in groin or medial thigh). CT/MRI to diagnose

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40
Q

What is a hiatus hernia?

A

Herniation of stomach through the diaphragm (the diaphragm should be at the level of the lower oesophageal sphincter and should be fixed in place).
Type 1: sliding
Type 2: rolling
Type 3: combination of rolling and sliding
Type 4: large opening with additional abdominal organs entering the thorax e.g. bowel, pancreas, omentum.
They present with dyspepsia.
Investigations: CXR, CT, endoscopy, barium swallow.
Management: medical management of GORD or surgical repair: laparoscoping fundoplication

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41
Q

How do hiatus hernia present

A

Dyspepsia with:
Heartburn
Reflux
Burping
Bloating
Halitosis

Intermittent so investigations (CXR, CT, endoscopy, barium swallow) may be normal

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42
Q

What is the management of a hiatus hernia?

A

Medical management of GORD
Surgical repair: laparoscoping fundoplication to narrow the oesophageal sphincter

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43
Q

What are haemorrhoids?

A

Enlarged anal vascular cushions, usually located at 3, 7 and 11 o’clock

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44
Q

How are haemorrhoids classified?

A

1st degree: no prolapse
2nd degree: prolapse on straining, return on relaxing
3rd degree: prolapse on straining, do not return on relaxing but can be pushed back
4th degree: prolapsed permanently

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45
Q

Are haemorrhoids painful?

A

No, unless they become thromboses (purplish, very tender swollen lumps around anus, unlikely to be able to perform PR)

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46
Q

What are the differentials for haemorrhoids?

A

Anal fissure
Diverticulosis
IBD
Colorectal cancer

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47
Q

What are the investigations for haemorrhoids?

A

PR
Proctoscopy

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48
Q

What is the management of haemorrhoids

A

Topical: anusol, anusol HC (with hydrocortisone), germoloids cream (contains lidocaine), proctosedyl ointment (hydrocortisone and cinchocaine)
Non-surgical: rubber band ligation, injection sclerotherapy, infra-red coagulation, bipolar diathermy
Surgical: haemorrhoids artery ligation during proctoscopy, haemorrhoidectomy (may result in incontinence), stapled haemorrhoidectomy.

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49
Q

What are the main branches of the abdominal aorta?

A

Coeliac artery (stomach, part of duodenum, liver, pancreas, biliary system, spleen)
Superior mesenteric artery (distal part of duodenum, first half of transverse colon)
Inferior mesenteric artery (last half of transverse colon, rectum)

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50
Q

What causes mesenteric iscahemia?

A

Atherosclerosis, same risk factors as CVD.

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51
Q

What is the pain like in mesenteric ischaemia?

A

Central colicky pain after eating

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52
Q

What are the clinical signs of mesenteric ischaemia?

A

Abdominal bruit may be heard

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53
Q

What is the diagnostic test for mesenteric ischaemia?

A

CT angiography

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54
Q

What is the first line investigation for mesenteric ischaemia?

A

VBG for lactate

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55
Q

What is the management of mesenteric ischaemia?

A
  1. Endovascular procedures e.g. percutaneous mesenteric artery stenting
  2. Open surgery (endarterectomy, re-implantation, bypass surgery)
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56
Q

What artery is blocked in acute mesenteric iscahemia?

A

Superior mesenteric artery (usually by a thrombus)

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57
Q

What is a risk factor for acute mesenteric ischaemia?

A

AF

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58
Q

What is the diagnostic investigation for acute mesenteric ischaemia?

A

Contrast CT

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59
Q

What is the management for acute mesenteric ischaemia?

A

Remove necrotic bowel
Remove/bypass thrombus (open/endovascular)

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60
Q

What is shown on a VBG in acute mesenteric ischaemia?

A

Metabolic acidosis
High lactate

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61
Q

What is diverticulosis?

A

Presence of diverticular without inflammation or infection

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62
Q

What is diverticular disease?

A

When patients start experiencing symptoms

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63
Q

What is diverticulitis?

A

Inflammation/infection of diverticula

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64
Q

Where is the pain felt in diverticular disease?

A

Lower left abdominal pain

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65
Q

What is the management of diverticular disease?

A

Increased fibre in diet and weight loss if appropriate.
Bulk forming laxatives e.g. ispaghula husk (avoid stimulant e.g. Senna).
Surgery to remove affected areas.

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66
Q

How do diverticula form?

A

Weakness in the circular muscle allows gaps to form which allows mucosa to herniate through.
Do not form in the rectum because this has an outer longitudinal muscle layer

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67
Q

Where does diverticulosis most commonly affect?

A

Sigmoid colon

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68
Q

How is acute diverticulitis treated?

A

If uncomplicated: oral co-amoxiclav for at least 5 days
If severe: nil by mouth, IV antibiotics, IV fluids, urgent CT, urgent surgery for complications

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69
Q

What is the fourth most prevalent cancer in the UK?

A

Bowel

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70
Q

What are three risk factor conditions for bowel cancer?

A

Familial adenomatous polyposis (FAP): patients should have prophylactic removal of entire large bowel
Hereditary nonpolyposis colorectal cancer
IBD

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71
Q

What is the screening for bowel cancer?

A

Faecal immunochemical test: 60-74 every 2 years but now expanding to 50-74.
If positive, sent for colonoscopy.
Can also be used if:
>50 with unexplained weight loss
<60 with change in bowel habit

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72
Q

How are patients with FAP, FNPCC and IBD monitored for bowel cancer?

A

Offered colonoscopy at regular intervals

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73
Q

What is the gold standard investigation for bowel cancer?

A

Colonoscopy + biopsy

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74
Q

How do you monitor for relapse in bowel cancer?

A

Carcinoembryonic antigen (CEA). Not useful for screening

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75
Q

What are the management options for bowel cancer?

A

Surgical resection
Chemotherapy
Radiotherapy
Palliative care

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76
Q

How can bowel cancer present on blood tests?

A

Iron deficiency anaemia (microcytic anaemia with low ferritin)

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77
Q

How long are patients with surgical resection for bowel cancer followed up?

A

Around 3 years post curative surgery for serum CEA and CT TAP

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78
Q

How is bowel cancer graded?

A

TNM classification
T1-T4
N0-N2
M0-M1

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79
Q

What is a right hemicolectomy?

A

Removal of caecum, ascending and proximal transverse colon

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80
Q

What is a left hemicolectomy?

A

Removal of distal transverse colon and descending colon

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81
Q

What is a high anterior resection?

A

Removal of the sigmoid colon

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82
Q

What is a low anterior resection?

A

Removal of sigmoid colon and upper rectum but sparing the lower rectum and anus

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83
Q

What is an abdomino-perineal resection?

A

Removal of the anus and rectum (+/- sigmoid colon) with suturing over the anus and permanent colostomy

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84
Q

What is a Hartmann’s procedure?

A

Usually emergency.
Removal of rectosigmoid colon and creation of colostomy (permanent or reversed later)

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85
Q

What is the difference between a colostomy and an ileostomy?

A

Colostomy solid stool and ileostomy more liquid.
Colostomy flush to skin and ileostomy spouted.
Colostomy found in left iliac fossa and ileostomy in right iliac fossa.

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86
Q

What is the difference between a closed stoma and loop stoma?

A

A loop is usually temporary and a closed is usually used when the condition is irreversible.

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87
Q

What is a panproctocolectomy?

A

Total colectomy with removal of large bowel, rectum and anus (treatment of IBD and FAP).

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88
Q

What are most gallstones made of?

A

Cholesterol

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89
Q

What does fatty food trigger biliary colic?

A

Fat entering the digestive system causes cholecystokinin (CCK) secretion from the duodenum which triggers contraction of the gallbladder and biliary colic

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90
Q

What are the risk factors for gallstones?

A

F at
F orty
F air
F emale

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91
Q

Where do gallstones get stuck to cause biliary colic?

A

Gallbladder or cystic duct

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92
Q

What is the incision in a cholecystectomy?

A

Kocher subcostal incision

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93
Q

What is the most sensitive imagine for gallstones?

A

Abdominal US

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94
Q

What is shown on US in acute cholecystitis?

A

Thickened gallbladder wall
Fluid around gallbladder
Stones/sludge

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95
Q

How can gallstones be removed?

A

ERCP
Laparoscopic cholecystectomy

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96
Q

When is MRCP used for gallstones?

A

If US negative for a stone but there is bile duct dilatation or raised bilirubin suggestive of an obstruction

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97
Q

What can be done during an ERCP?

A

Inject contrast and take X-rays
Sphincterectomy if sphincter of Oddi is dysfunctional
Clear stones from ducts
Insert stents for strictures/tumours
Take biopsies of tumours

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98
Q

What is a key complication of ERCP?

A

Cholangitis and pancreatitis

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99
Q

Where other than the liver is ALP (alkaline phosphatase) produced?

A

Bone
Placenta during pregnancy

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100
Q

Which LFTs are good markers of hepatocellular injury?

A

The aminotransferases: ALT (alanine transferase) and AST (aspartate aminotransferase)

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101
Q

What do LFTs look like in an “obstructive pattern”?

A

Big raise in ALP compared to ALT and AST

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102
Q

What do LFTs look like in a “hepatic pattern”?

A

Big raise in ALT and AST compared to ALP

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103
Q

What is a cholecystectomy?

A

Drain in gallbladder

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104
Q

What is cholelithiasis?

A

Gallstones are present

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105
Q

What is cholecolithiasis?

A

Gallstones are in bile duct

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106
Q

What causes cholecystitis?

A

Blockage of the cystic duct, preventing the gallbladder from draining.

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107
Q

What is the sign in acute cholecystitis?

A

Murphy’s sign: place hand in RUQ and ask patient to take a deep breath in. Gallbladder will move downwards during inspiration and come into contact with hand which causes sudden stopping of inspiration

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108
Q

What imaging is used in acute cholecystitis?

A

Abdominal US
MRCP if US negative

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109
Q

What is the definitive management of acute cholecystitis?

A

Cholecystectomy usually performed during acute admission within 72 hours.

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110
Q

What is the initial management of acute cholecystitis?

A

Nil by mouth
IV fluids
Antibiotics
NG tube if vomiting

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111
Q

What is acute cholangitis?

A

Inflammation of the bile ducts

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112
Q

What is Charcot’s triad

A

For acute cholangitis:
1. RUQ pain
2. Fever
3. Jaundice

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113
Q

What is the most sensitive imagine for acute cholangitis?

A

Endoscopic US (best)
MRCP
CT
Abdominal US

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114
Q

What is the management of acute cholangitis?

A

ERCP with:
Cholangio-pancreatography (contrast and X-ray imagine)
Sphincterectomy
Stone removal
Balloon dilatation
Biliary stenting

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115
Q

What is the management of acute cholangitis if ERCP not suitable?

A

Percutaneous transhepatic cholangiogram (radiologically guided insertion of drain)

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116
Q

What are the main causes of acute cholangitis?

A

Obstruction e.g. gallstone in CBD
Infection introduced during ERCP

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117
Q

What are the main organisms acute cholangitis?

A

Eschericia coli
Klebsiella species
Enterococcus species

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118
Q

What are the majority of cholangiocarcinomas?

A

Adenocarcinomas

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119
Q

Where is the most common site for a cholangiocarcinoma?

A

Perihilar region when the L and R hepatic duct have joined to become the common hepatic duct just after leaving the liver

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120
Q

Which condition is a major risk factor for cholangiocarcinoma?

A

Primary sclerosing cholangitis

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121
Q

Which condition is a major risk factor for primary sclerosing cholangitis?

A

Ulcerative colitis

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122
Q

How does cholangiocarcinoma present?

A

Obstructive jaundice: pale stools, dark urine, generalised itching
RUQ pain
Weight loss
Hepatomegaly
Palpable gallbladder

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123
Q

What is Courvoiser’s law?

A

Palpable gallbladder + jaundice = unlikely to be gallstones. Cause is usually pancreatic/cholangiocarcinom

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124
Q

Which two conditions does obstructive jaundice indicate?

A

Head of pancreas tumour
Cholangiocarcinoma (less common)

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125
Q

Which tumour marker is raised in cholangiocarcinoma?

A

CA 19-9

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126
Q

What are the diagnostic investigations for primary sclerosing cholagnitis?

A

MRCP
ERCP (+biopsy if tumour)

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127
Q

What is the management of cholangiocarcinoma?

A

Most cases palliative with:
Stents to relive obstruction
Surgery to bypass obstruction
Palliative chemotherapy/radiotherapy

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128
Q

What are the majority of pancreatic cancers?

A

Adenocarcinomas

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129
Q

What does a HOP cancer obstruct to cause jaundice?

A

Common bile ducts

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130
Q

Which hereditary condition is associated with pancreatic cancer?

A

Hereditary non-polyposis colorectal carcinoma

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131
Q

What is the “double duct sign”?

A

Dilatation of CBD and pancreatic ducts in pancreatic cancer

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132
Q

Where is a palpable mass felt in pancreatic cancer?

A

Epigastric region

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133
Q

What is a sign of pancreatic cancer?

A

Trosseua’s sign of malignancy (migratory thrombophlebitis)

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134
Q

What is diagnostic for pancreatic cancer?

A

High resolution CT scan and histology from biopsy.
Biopsy taken through skin (percutaneous) under USS guidance or during endoscopy under USS guidance

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135
Q

What is the tumour marker raised in pancreatic cancer?

A

CA19–9 (carbohydrate antigen)

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136
Q

What is the management of pancreatic cancer?

A

Mostly palliative with:
Stents to relieve obstruction
Surgery to bypass obstruction
Palliative chemotherapy/radiotherapy.

A small amount may have surgery if small HOP:
Pancreatectomy
Whipple’s or modified Whipple’s (preserved pylorus)

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137
Q

What is primary sclerosing cholangitis?

A

Intrahepatic and extrahepatic bile ducts become inflamed and damaged, developing strictures that obstruct bile flow out of liver and into intestines

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138
Q

Which LFT is particularly raised in primary sclerosing cholangitis?

A

ALP

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139
Q

What is the diagnostic investigation for primary sclerosing cholangitis?

A

MRCP

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140
Q

Other than MRCP what investigation should be performed for primary sclerosing cholangitis?

A

Colonoscopy to look for UC.

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141
Q

What is the management of primary sclerosing cholangitis?

A

No definitive
ERCP with stents for strictures
Liver transplant in advanced
Replacement of fat soluble vitamins (A, D, E and K)

142
Q

What can be used for pruritus?

A

Colestyramine (reduces intestinal absorption of bile acids)

143
Q

What are the causes of pancreatitis?

A

I diopathic
G allstones*
E thanol*
T rauma
S teroids
M umps
A utoimmune
S scorpion sting
H yperlipidaemia
E RCP*
D rugs: furosemide, thiazide diuretics, azathioprine

144
Q

What is the most common cause of chronic pancreatitis?

A

Alcohol

145
Q

What are the complications of chronic pancreatitis?

A

Chronic epigastric pain
Loss of exocrine function (lack of enzymes e.g. lipase)
Loss of endocrine function (insulin)
Obstruction of pancreatic juice and bile
Formation of pseudocysts or abscesses

146
Q

Where do gallstones get trapped to cause pancreatitis?

A

Ampulla of Vater

147
Q

What score is used in pancreatitis?

A

Glasgow Scale
P aO2 <8
A ge >55
N eutrophils
C alcium <2
R urea >16
E enzymes (LDH>600, AST, ALT>200)
A albumin <32
S ugar (glucose) >10

148
Q

How raised is amylase in pancreatitis?

A

> 3 times the upper limit

149
Q

How is diagnosis for pancreatitis made?

A

Clinical

150
Q

What is the mnemonic for Crohn’s?

A

“Crows” NESTS:
N o blood or mucus
E ntire GI tract affected
S kip lesions on endoscopy
T erminal ileum most affected and transmural inflammation
S moking is a risk factor

151
Q

What is seen on endoscopy in Crohn’s?

A

Granulomas
Increased goblet cells

152
Q

What is the diagnostic investigation for Crohn’s?

A

Colonoscopy with multiple intestinal biopsies

153
Q

What is the initial test for IBD?

A

Faecal calprotectin stool

154
Q

How do you treat a flare of Crohn’s?

A
  1. Steroids: oral prednisolone or IV hydrocortisone
    If not adequate:
    Azathioprine
    Mercaptopurine
    Methotrexate
    Infliximab
    Adalimumab
155
Q

How do you maintain remission in Crohn’s?

A
  1. Azathioprine or Mercaptopurine
    Surgical:
    Resect distal ileum
    Treat strictures
    Treat fistulas
156
Q

What are the extra intestinal manifestations of IBD?

A

Erythema nodosum
Pyoderma gangrenosum
Enterohepathic arthritis
Primary sclerosing cholangitis (UC)
Red eye conditions
Finger clubbing

157
Q

What is seen on endoscopy in UC?

A

Crypt abscesses
Depletion of goblet cells

158
Q

What is the mnemonic for UC?

A

“You see” (UC) CLOSEUP:
C continuous inflammation
L limited to colon and rectum
O nly superficial mucosa
S moking may be protective
E Crete blood and mucus
U se aminosalicylates
P primary sclerosing cholangitis

159
Q

How do you treat a mild flare of UC?

A
  1. Rectal aminosalicylate e.g. PR mesalazine
  2. Oral salicylate
  3. Oral or PR corticosteroid e.g. prednisolone
160
Q

How do you treat a severe flare of UC?

A
  1. IV steroids
    IV ciclosporin
    Infliximab
    Surgery: panproctocolectomy with permanent ileostomy.
161
Q

How do you maintain remission in UC?

A
  1. Aminosalicylate e.g. oral or PR mesalazine
    Azathioprine oral or mercaptopurine oral if following a severe prolapse or >= 2 exacerbations in a year
162
Q

What is portal hypertension?

A

Fibrosis increases the resistance of blood flow through the liver, increasing the resistance in the vessels leading to the liver in the portal system.

163
Q

What are the four most common causes of liver cirrhosis?

A
  1. Alcohol
  2. NAFLD
  3. Hepatitis B
  4. Hepatitis C.

Other:
Wilson’s
Haemochromatosis
Autoimmune hepatitis
Primary biliary cirrhosis
Alpha-1 antitrypsin deficiency
CF
Drugs e.g. amiodarone, methotrexate and sodium valproate

164
Q

Why do you get splenomegaly in liver cirrhosis?

A

Portal hypertension

165
Q

What is involved in a non-invasive liver screen?

A

US liver: used to diagnose fatty liver
Hepatitis B and C
Autoantibodies: autoimmune hepatitis, PBC, PSC
Immunoglobulins: autoimmune hepatitis, PBC
Ceruloplasmin: Wilson’s disease
Alpha-1 antitrypsin levels
Ferritin and transferrin: haemochromatosis

166
Q

Which antibodies are relevant to liver disease?

A

Antinuclear antibodies
Smooth muscle antibodies
Antimitochondrial antibodies
Antibodies to liver kidney microsome type 1

167
Q

Why is albumin low in liver cirrhosis?

A

Reduced synthetic function of liver

168
Q

Why is prothrombin time increased in liver cirrhosis?

A

Reduced production of clotting factors

169
Q

Why does hyponatraemia occur in liver cirrhosis?

A

Fluid retention

170
Q

What is a tumour marker for hepatocellular carcinoma?

A

Alpha-fetoprotein

171
Q

What is the first line blood test in assessing fibrosis in NAFLD?

A

Enhanced liver fibrosis blood test

172
Q

What imaging is used to diagnose NAFLD?

A

US (fatty changes appear as increased echogenicity)

173
Q

What are signs of liver cirrhosis on US?

A

Nodularity of surface of the liver
Enlarged portal vein
Ascites
Splenomegaly

174
Q

What investigation is used to assess the degree of fibrosis in liver cirrhosis?

A

“FibroScan” (transient elastography) used in patients at risk of liver cirrhosis

175
Q

What is diagnostic for liver cirrhosis?

A

Liver biopsy

176
Q

How do you monitor for complications in liver cirrhosis?

A

Model for end stage liver disease score every 6 months
US and AFP every 6 months for hepatoceullular carcinoma
Endoscopy every 3 years for oesophageal varices

177
Q

When is a liver transplant indicated?

A

Decompensated:
A scites
H epatic encephalopathy
O oesophageal varices bleed
Y allow (jaundice)

178
Q

What score can be used to assess the severity of liver cirrhosis and prognosis?

A

Child-Pugh score

179
Q

What is a systemic complication of acute pancreatitis?

A

Acute respiratory distress syndrome

180
Q

Where does Crohn’s most commonly affect?

A

Terminal ileum

181
Q

What are long term effects of Crohn’s?

A

Perianal abscess and fistula
Small bowel obstruction
Malnutrition

182
Q

How does infliximab work in Crohn’s?

A

Directed against tumour necrosis factor

183
Q

What condition is associated with oesophageal varices?

A

Liver cirrhosis

184
Q

How does liver cirrhosis cause oesophageal varices?

A

Venous portal hypertension

185
Q

What type of medication is terlipressin?

A

Vasporessin analgoue

186
Q

What are the endoscopic treatment of oesophageal varices?

A

Banding of varices, adrenaline, sclerotherapy

187
Q

Where do collaterals occur between the portal and systemic venous systems?

A

Distal oesophagus (oesophageal varices)
Anterior abdominal wall (caput medusae)

188
Q

What is prophylaxis for bleeding in stable oesophageal varices?

A
  1. BB non-selective e.g. propranolol
  2. Variceal band ligation if BB CI
189
Q

What has been shown to reduce mortality in bleeding oesophageal varices?

A

Prophylactic broad spectrum antibiotics

190
Q

What are causes of upper GI bleeding?

A

Peptic ulcer (most common)
Mallory Weiss tear
Oesophageal varices
Stomach cancers

191
Q

Why do you get melaena in upper GI bleed?

A

Digested blood

192
Q

What score is used in upper GI bleeding?

A

Glasgow Blatchford score used initially
Rockall score used after endoscopy

193
Q

What is shown on bloods for upper GI bleeding?

A

Low Hb: may be normal initially as not had time to drop
Raised urea: significantly raised compared to creatinine

194
Q

What is the initial management of an upper GI bleed?

A

A BCDE approach
B loods (Hb, urea, coagulation, LFTs, crossmatch 2 units of blood)
A access (2 large bore cannulas)
T ransfusions
E endoscopy within 24 hours
D rugs (stop anticoagulants and NSAIDs)

195
Q

What is a group and save?

A

Lab checks the patient’s blood group and saves a blood sample to match to blood if needed

196
Q

What is a crossmatch?

A

Where the lab allocates units of blood, tests that it is compatible and keeps it ready in the fridge

197
Q

What type of blood is given in massive bleeding?

A

Blood
Platelets
Fresh frozen plasma (clotting factors)

198
Q

What medications are used in oesophageal variceal bleeding?

A

Terlipressin
Broad spectrum antibiotics

199
Q

What are the types of peptic ulcer?

A

Gastric and duodenal

200
Q

What are risk factors for peptic ulcers?

A

Helicobacter pylori
NSAIDs
They disrupt the mucus barrier (mucosa) that secretes bicarbonate which neutralises the stomach acid.

Increasing stomach acid:
Stress
Alcohol
Caffeine
Smoking
Spicy foods

201
Q

Which drugs increase the risk of bleeding from a peptic ulcer?

A

NSAIDs
Aspirin
Anticoagulants
Steroids
SSRIS

202
Q

What is Zollinger-Ellison syndrome?

A

Excessive quantities of gastrin secreted from a duodenal or pancreatic tumour. Gastrin stimulates the stomach to produce stomach acid, resulting in severe peptic ulcers.

Gastrin secreting tumours can be associated with MEN 1

203
Q

How do you differentiate between gastric and duodenal ulcer?

A

Pain of eating worsens gastric ulcer but improves with duodenal ulcer (gets worse after 2-3 hours)

204
Q

What test can be performed during endoscopy to check for H Pylori?

A

Rapid urease test (CLO)
H Pylori bacteria produce urease enzymes which convert urea to ammonia, making the solution more alkaline which can be tested for

205
Q

What type of bacteria is Helicobacter pylori?

A

Gram negative aerobic bacteria

206
Q

What is the pathophysiology of H Pylori?

A

Produces toxins and ammonium hydroxide which leads to gastric mucosal damage.

207
Q

How long must you stop a PPI for before H Pylori test?

A

2 weeks
Antibiotics for 4 weeks

208
Q

What is the treatment for H Pylori?

A

7 days of:
PPI
Amoxicillin
Clarithromycin

209
Q

What are the initial investigations for H Pylori?

A

Urea breath test using radio labelled carbon 13
Stool antigen test
H pylori antigen test (blood)

210
Q

What is the lining of the oesophagus?

A

Squamous epithelial lining (more sensitive to stomach acid)

211
Q

What is the lining of the stomach?

A

Columnar epithelium (more protected against stomach acid)

212
Q

What are the red flag symptoms for dyspepsia?

A

Dysphagia
>55
Weight loss
Treatment resistant
Anaemia
Upper abdominal mass

213
Q

What is the medical management of GORD?

A

Antacids e.g. Gaviscon
PPI
Histamine H2 receptor antagonists e.g. famotidine

214
Q

What is a surgical management of GORD?

A

Laparoscopic fundoplication (tying funds of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter).

215
Q

What is a complication of GORD?

A

Barret’s oesophagus

216
Q

What happens in Barrett’s oesophagus?

A

Epithelium changes from squamous to columnar (metaplasia)

217
Q

What is the treatment of Barrett’s oesophagus?

A

Endoscopic monitoring for progression to adenocarcinoma.
PPI.
Endoscopic ablation e.g. radiofrequency.

218
Q

What causes ascites?

A

Increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and other organs into the peritoneal cavity.

219
Q

What type of fluid is ascites?

A

Transudative (low protein)

220
Q

How do ascites cause sodium retention?

A

There is a drop in circulating volume caused by fluid loss into the peritoneal cavity which caused reduce blood pressure in the kidneys. The kidneys respond to this by releasing renin which leads to increased aldosterone secretion. This causes the reabsorption of fluid and sodium in the kidneys.

221
Q

How are ascites managed?

A

Low sodium diet
Aldosterone antagonists
Paracentesis (ascitic tap or drain)
Prophylactic antibiotics when there is <15g protein in the ascitic fluid

222
Q

How are refractory ascites treated?

A

Transjugular intrahepatic portosystemic shunt
Liver transplantation

223
Q

What are the most common bacteria in SBP?

A

Eschericial coli
Klebsiella pneumonoiae

224
Q

What antibiotic is used for spontaneous bacterial peritonitis?

A

IV broad spectrum e.g. piperacillin with tazobactam

225
Q

What do patients require after an episode of SBP?

A

Antibiotic prophylaxis e.g. ciprofloxacin

226
Q

How does portal hypertension cause hepatorenal syndrome?

A

Portal hypertension causes vessels to release vasodilators. There is reduced blood pressure to the kidneys so they produce renin. This causes vasoconstriction of the kidney blood vessels whilst they are also receiving low systemic blood pressure.

227
Q

What is the treatment of hepatorenal syndrome?

A

Liver transplant

228
Q

What is the key toxin in hepatic encephalopathy?

A

Ammonia

229
Q

How is hepatic encephalopathy treated?

A

Lactulose (2-3 soft stools per day): to clear ammonia before it is absorbed, makes the intestine more acidic so kills ammonia-producing bacteria
Antibiotics e.g. rifaximin to reduce the number of intestinal bacterial producing ammonia

230
Q

How does ammonia get from the liver to the brain?

A

Liver does not metabolise it as it should.
Collateral vessels between the portal and systemic circulation mean the ammonia bypasses the liver and enters the systemic circulation directly.

231
Q

How long do symptoms of IBS need to be present for a diagnosis?

A

6 months

232
Q

What is the diet recommended for IBS?

A

FODMAP

233
Q

What is the first line medication for diarrhoea in IBS?

A

Loperamide

234
Q

What is the first line medication for constipation in IBS?

A

Bulk forming e.g. ispaghula husk
Linaclotide is specialist if this does not work

235
Q

Which laxative should be avoided in IBS?

A

Lactulose (can cause bloating)

236
Q

What medications are used for cramps in IBS?

A

Antispasmodics e.g. mebeverine, alverine, hyoscine butylbromide

237
Q

What are other management options for IBS if first line do not work?

A

Low dose tricyclic antidpressant
SSRI
CBT.

238
Q

Which antibodies are involved in coeliac?

A

Anti-tissue transglutaminase antibodies
Anti-endomysial antibodies
Anti-deamidated gliadin peptide antibodies (anti-DGP)

239
Q

Where does coeliac disease affect?

A

Small bowel, particularly the jejunum

240
Q

What is the pathophysiology of coeliac disease?

A

The villi which increase the surface area and help with nutrient absorption are destroyed, resulting in malabsorption.

241
Q

What must all new T1DM patients be tested fir?

A

Coeliac disease
Thyroid disease

242
Q

Which HLA genotypes is coeliac related to?

A

HLA-DQ2
HLA-DQ8

243
Q

Which rash is associated with coeliac disease?

A

Dermatitis herpetiformis (typically on abdomen, blistering itchy rash)

244
Q

What are the first line blood tests in coeliac disease?

A

Total IgA: some patient shave IgA deficiency which will cause antibody test to be negative
Anti-TTG

245
Q

What are the typical biopsy findings for coeliac disease?

A

Crypt hyperplasia
Villous atrophy

246
Q

How can coeliac disease present neurologically?

A

Peripheral neuropathy
Cerebellar ataxia
Epilpesy

247
Q

What vaccination should patients with coeliac disease receive?

A

Pneumococcal with booster every 5 years and annual flu vaccination due to hyposplenism

248
Q

What are the consequences of continuing to eat gluten in coeliac disease?

A

Hyposlpenism
Ulcerative jejunitis
Enteropathy-associated T cell lymphoma
Non-Hodkin lymphoma
Small bowel adenocarcinoma

249
Q

Why does anaemia occur in coeliac disease?

A

Malabsorption and deficiency of iron, B12 or folate

250
Q

What does meleana suggest in upper GI bleed?

A

Large blood loss

251
Q

How do you investigate a GI perforation?

A

Erect CXR. Would show free air below the diaphragm

252
Q

How can GORD cause a wheeze?

A

Inhalation of small amounts of gastric contents

253
Q

Which condition is a risk factor for GORD?

A

Hiatus hernia

254
Q

What is the gold standard investigation for proving reflux?

A

Oesophageal pH manometry

255
Q

What is dumping syndrome?

A

Food, especially food high in sugar, moves from your stomach into your small bowel too quickly after you eat. Sometimes called rapid gastric emptying, dumping syndrome most often occurs as a result of surgery on your stomach or esophagus.

256
Q

What is bilirubin a breakdown of?

A

Haemoglobin

257
Q

Why does conjugated bilirubin appear in the urine and not unconjugate bilirubin doesn’t?

A

Bilirubin that has conjugated in the liver is water soluble

258
Q

What does primary biliary cholangitis affect?

A

The small bile ducts inside the liver (intrahepatic ducts)

259
Q

What are the signs of primary biliary cholangitis?

A

Raised bile acids in the blood causing itching (less bile acids in the GI tract so malabsorption of fat and greasy stools)
Raised bilirubin in the blood causes jaundice (less bilirubin in GI tract results in pale stools and more excreted in Rubin causes dark urine)
Raised cholesterol causes xanthelasma (xanthomas are large nodular deposits of cholesterol in the skin or tendons).

260
Q

What condition is primary biliary cholangitis associated with?

A

Sjogrens syndrome

261
Q

What are the clinical signs of primary biliary cholangitis?

A

Xanthoma and xanthelasma
Hepatomegaly
Signs of liver cirrhosis and portal hypertension in end-stage e.g. splenomegaly and ascites
Clubbing
Excoriations.

262
Q

What are the two main investigations in primary biliary cholangitis?

A

Raised ALP
Anti-mitochondrial antibodies

263
Q

What is the management of primary biliary cholangitis?

A

Ursodeoxycholic acid
Replacement of fat soluble vitamins

264
Q

What is the most significant complication of primary biliary cholangitis?

A

Portal hypertension and hepatocellular carcinoma

265
Q

What is the stepwise progression of alcoholic liver disease?

A

Alcoholic fatty liver to alcoholic hepatitis to cirrhosis

266
Q

What is binge drinking?

A

6 or more units for women or 8 or more units for men

267
Q

What do blood tests show in alcoholic liver disease?

A

Raised MCV
Raised gamma-glutamyl transferase (GGT)
Raised bilirubin in cirrhosis
Low albumin due to synthetic function of the liver
Increased prothrombin time due to synthetic function of the liver.

268
Q

How do fatty changes show on US in early alcoholic fatty liver?

A

Increased echogenicity

269
Q

What investigation is diagnostic for alcoholic liver disease?

A

Liver biopsy

270
Q

What effect does alcohol have on the body?

A

Stimulates GABA receptors which have a relaxing effect. Inhibits glutamate receptors which is an excitatory neurotransmitter

271
Q

How does chronic alcohol effect the body?

A

The GABA system becomes down-regulated and the glutamate system becomes up-regulate to balance the effects of alcohol. When the alcohol is removed, the GABA system under-functions and the glutamate system over functions causing extreme excitability and excessive adrenalin-related activity

272
Q

What happens 6-12 hours after last alcoholic drink?

A

Tremor, sweating, headache, craving, anxiety

273
Q

What happens 12-24 hours after last alcoholic drink?

A

Hallucinations

274
Q

What happens 24-48 hours after last alcoholic drink?

A

Seizures (peak onset at 36 hours)

275
Q

What happens at 24-72 hours after last alcoholic drink?

A

Delirium tremens

276
Q

What is the CAGE questionnaire?

A

C ut down? Do you think you should?
A nnoyed? Do you get annoyed about others commenting on your drinking?
G guilty?
E ye opener? Do you drink in the morning to help your hangover or nerves?

277
Q

What questionnaire is used to screen for harmful alcohol use?

A

AUDIT (Alcohol Use Disorders Identification Test)

278
Q

What is the inheritance pattern for haemachromatosis?

A

Autosomal recessive with gene on chromosome 6

279
Q

What is the pathophysiology of haemochromatosis?

A

Excessive total body iron and deposition of iron in tissues (iron storage disorder).

280
Q

What are the symptoms of haemochromatosis?

A

Chronic tiredness
Joint pain
Pigmentation
Testicular atrophy
Erectile dysfunction
Amenorrhoea
Cognitive symptoms
Hepatomegaly

281
Q

What is the first line investigation for haemochromatosis?

A

Serum ferritin

282
Q

Is transferrin saturation high or low in haemochromatosis?

A

High

283
Q

What investigation is diagnostic for haemochromatosis?

A

Genetic testing

284
Q

What is the management of haemochromatosis?

A

Venesection weekly

285
Q

What are the stages of non-alcohol fatty liver disease?

A

NAFLD
Non-alcoholic steatohepatitis
Fibrosis
Cirrhosis

286
Q

Which conditions does NAFLD share risk factors with?

A

Cardiovascular disease and diabetes

287
Q

What investigation is diagnostic for NAFLD?

A

US

288
Q

Which LFT is most often the first raised in NAFLD?

A

ALT

289
Q

What is the gold standard test for NAFLD?

A

Liver biopsy

290
Q

What is the first line investigation for assessing fibrosis in NAFLD?

A

Enhanced liver fibrosis blood test.
If negative (<10.51) then repeat every 3 years.
If indicates severe fibrosis, use “FibroScan” (transient elastography)

291
Q

What are scores for assessing firbrosis in NAFLD?

A

NAFLD Fibrosis Score
Fibrosis 4 (FIB4)

292
Q

What is the management of NAFLD?

A

Lifestyle

293
Q

What are the hereditary causes of liver cirrhosis?

A

Haemochromatosis
Alpha-1 antitrypsin deficiency
Wilson’s

294
Q

What are the acquired causes of liver cirrhosis?

A

Chronic alcohol abuse
Chronic viral hepatitis
Autoimmune hepatitis
Primary biliary cirrhosis
Idiopathic
Venous obstruction

295
Q

What are signs of chronic liver disease on examination?

A

Leuconychia
Clubbing
Palmar erythema
Dupuytren’s contracture
Spider naevia
Gynaecomastia
Hepatosplenomegaly
Ascites
Atrophic testes

296
Q

What are complications of liver cirrhosis?

A

Coagulopathy
Encephalopathy
Hypoalbuminaemia
Sepsis
Spontaneous bacterial peritonitis
Hypoglycaemia
Ascites
Oesophageal varices

297
Q

How are ascites treated?

A

Fluid restriction
Diuretics
Abdominal paracentesis (ascitic tap)
Albumin infusion

298
Q

What investigations should be ordered on ascitic fluid?

A

White cell count
MC&S
Cytology
Albumin/LDH/glucose

299
Q

Why is lactulose used in hepatic encephalopathy?

A

Increases bowel transit reduces the number of nitrogen producing bacteria in the gut.

300
Q

Which conditions cause GI malabsorption?

A

Coeliac
Crohn’s
Cystic fibrosis
Chronic pancreatitis
Dumping syndrome

301
Q

What is the commonest form of gluten?

A

Wheat

302
Q

Which autoimmune conditions are associated with Coeliac?

A

T1DM
Thyroid disease

303
Q

Name two cancers associated with coeliac disease.

A

GI T cell lymphoma
Gastric
Oesophageal

304
Q

Which viruses cause gastroenteritis?

A

Rotavirus
Norovirus
Adenovirus

305
Q

What is the inheritance pattern of Wilson’s?

A

Autosomal recessive, gene on chromosome 13

306
Q

How can Wilson’s disease present?

A

Copper deposition in the liver: eventually leads to cirrhosis
Copper deposition in the CNS: tremor, dysarthria, dystonia, PD, abnormal behaviour, cognitive impairment
psychsos
Kayser-Fleischer rings
Haemolytic anaemia

307
Q

What is the first line investigation for Wilson’s?

A

Serum caeruloplasmin (will be low in Wilson’s): the protein that carries copper in the blood

308
Q

What is the characteristic sign on MRI brain in Wilson’s?

A

Double panda sign

309
Q

What is the management of Wilson’s?

A

Copper chelation:
1. Penicillamine
Trientine.

Other treatments”
Zinc salts (inhibit copper absorption in the GI tract)
Liver transplantation.

310
Q

Which LFTs are raised in autoimmune hepatitis?

A

ALT and AST.

311
Q

What are the two types of autoimmune hepatitis?

A

Type 1: middle aged women, present less acutely with fatigue
Type 2: children or young people, presents more acutely with high transaminases and jaundice

312
Q

What are the antibodies in type 1 autoimmune hepatitis?

A

Anti-nuclear antibodies
Anti-smooth muscle antibodies
Anti-soluble liver antigen.

313
Q

What are the antibodies in type 2 autoimmune hepatitis?

A

Anti-liver kidney microsomes-1
Anti-liver cytosol antigen type 1

314
Q

What is the management of autoimmune hepatitis?

A

High dose steroids e.g. prednisolone
Other immunosuppressants e.g. azathioprine
Liver transplant in end stage liver disease (can reoccur in the new liver).

315
Q

What are common benign tumours of the liver?

A

Haemangiomas

316
Q

What is focal nodular hyperplasia?

A

Benign liver tumour made of fibrotic tissue. Can be related to oestrogen and OCP

317
Q

What is the main risk factor for hepatocellular carcinoma?

A

Liver cirrhosis

318
Q

How are patients with liver cirrhosis screened for hepatocellular carcinoma?

A

US
Alpha fetoprotein

319
Q

What are the management options for hepatocellular carcinoma?

A

Surgery
Liver transplant
Radiofrequency ablation
Microwave ablation
Transarterial chemoembolisation: interventional radiology procedure (a chemotherapy drug is injected into the hepatic artery feeding the tumour followed by embolisation)
Radiotherapy
Targeted drugs (e.g. kinase inhibitors and monoclonal antibodies)

320
Q

How is hepatitis A transmitted?

A

Faecal-oral route

321
Q

How is hepatitis B transmitted?

A

Blood/bodily fluids

322
Q

How is hepatitis C transmitted?

A

Blood

323
Q

How is hepatitis D transmitted?

A

Always with hepatitis B

324
Q

How is hepatitis E transmitted?

A

Faecal-oral route

325
Q

What are notifiable diseases?

A

All virus hepatitis infections

326
Q

Which of the viral hepatitis is the only non RNA virus?

A

Hepatitis B

327
Q

Which is the most common viral hepatitis worldwide?

A

Hepatitis A

328
Q

What is the diagnosis for hepatitis A?

A

IgM antibodies

329
Q

What type of virus is hepatitis B?

A

A double stranded DNA virus

330
Q

What does positive HBsAg suggest?

A

Active infection

331
Q

What does the e antigen HBeAg indicate?

A

A marker of viral replication and implies infectivity

332
Q

What does positive HBcAb indicate?

A

Past or current infection (depending on if IgM or IgG positive)

333
Q

What does positive HBsAb indicate?

A

Vaccination or past/current infection.

334
Q

What does hepatitis B virus DNA indicate?

A

A direct count of the viral load

335
Q

What is the screening for hepatitis B?

A

HbcAb and HBsAg

336
Q

What is a vaccination for Hepatitis B?

A

HBsAg

337
Q

Which viral hepatitis can treatment be offered?

A

Hepatitis B: supportive/antivirals
Hepatitis C: direct acting antivirals e.g. sofosbuvir and daclarasvir
Hepatitis D: pegylated interferon alpha over at least 48 weeks

338
Q

What are the investigations for hepatitis C?

A

First line: hepatitis C antibody
Hepatitis C RNA used to confirm diagnosis, calculate the viral load and identify the genotype

339
Q

Which hereditary condition is most associated with pancreatic cancer?

A

Hereditary non-polyposis colorectal carcinoma

340
Q

Where is a palpable mass found on examination in pancreatic cancer?

A

Epigastric area

341
Q

What is Trousseau’s sign of malignancy?

A

Migratory thrombophlebitis as a sign of pancreatic adenocarcinoma

342
Q

What is the “double duct” sign in pancreatic cancer?

A

Dilatation of CBD and pancreatic ducts

343
Q

What is diagnostic for pancreatic cancer?

A

High resolution CT scan + US guided biopsy (percutaneous or during endoscopy)

344
Q

What tumour marker is associated with pancreatic cancer?

A

CA 19-9 (carbohydrate antigen)

345
Q

What are risk factors for an anal fissure?

A

Constipation
Inflammatory bowel disease
Sexually transmitted infections e.g. HIV, syphilis, herpes.

346
Q

What are anal fissures?

A

Longitudinal or elliptical tears of the squamous lining of the distal anal canal.

347
Q

How is an acute anal fissure defined?

A

< 6 weeks

348
Q

How is an acute anal fissure managed?

A

Soften stool: high-fibre with high fluid intake
Bulk forming laxatives first line (lactulose if not tolerated)
Lubricants before defecation e.g. petroleum jelly
Topical anaesthetics
Analgesia.

349
Q

What is the management of a chronic anal fissure?

A

Acute techniques continued
Topical GTN first line
If topical GTN not effective after 8 weeks then secondary care referral for surgery (sphincterotomy) or botulinum toxin.

350
Q
A

Finals (11 decks)

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