Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI > GI Clinical 1 > Flashcards

GI Clinical 1 Flashcards

Diseases, treatments etc.

1
Q

What is oesophageal reflux?

A

Reflux of gastric acid into oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What happens to the squamous epithelium with oesophageal reflux?

A

It thickens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are some of the things that can happen to the oesophagus with severe reflux?

A

Ulceration, fibrosis, stricture formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What can happen as a result of fibrosis of the oesophagus?

A

Stricture formation, impaired motility, oesophageal obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is Barrett’s oesophagus?

A

Type of metaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is metaplasia of the oesophagus (Barrett’s oesophagus)?

A

Transformation from squamous epithelium to mucin-secreting columnar epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why can Barrett’s oesophagus be bad?

A

Pre-malignant condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the third most common cancer of the alimentary tract?

A

Oesophageal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the two histological types of oesophageal cancer?

A

Squamous carcinoma

Adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which histological type of cancer does Barrett’s oesophagus develop into?

A

Adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the risk factors for oesophageal squamous carcinoma?

A

Smoking, alcohol, dietary carcinogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the risk factors for oesophageal adenocarcinoma?

A

Barrett’s metaplasia, obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are some of the local effects of oesophageal cancer?

A

Obstruction, ulceration, perforation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the spread of oesophageal cancer?

A

Direct - to surrounding structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the lymphatic spread of oesophageal cancer?

A

To regional lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where does oesophageal cancer usually spread to via blood?

A

Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the prognosis for oesophageal cancer over 5 years?

A

Very poor, less than 15%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the three types of gastritis?

A 
Autoimmune (type A)
Bacterial (type B)
Chemical injury (type C)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is autoimmune gastritis?

A

Autoantibodies to parietal cells and intrinsic factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does autoimmune gastritis manifest?

A

Loss of specialised gastric epithelial cells -> decreased acid secretion and loss of intrinsic factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What effect does the loss of specialised gastric epithelial cells in autoimmune gastritis have on the stomach?

A

Decreased acid secretion and loss of intrinsic factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

During autoimmune gastritis, what effect does loss of intrinsic factor have on the stomach?

A

Pernicious anaemia which causes vitamin B12 deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the most common cause of pernicious anaemia?

A

Vitamin B12 deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the most common type of gastritis?

A

Bacterial gastritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What gram negative bacterium is bacterial gastritis related to?

A

Helicobacter pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Where is H.pylori found?

A

In gastric mucus on the surface of the gastric epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What affects does H.pylori have?

A

Produces acute and chronic inflammatory response

Increased acid production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What causes chemical gastritis?

A

Drugs (NSAIDS), alcohol, bile reflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How does peptic ulceration occur?

A

An inbalance between acid secretion and the mucosal barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Where does peptic ulceration occur?

A

Lower oesophagus, body and antrum stomach, 1st and 2nd parts of duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How is peptic ulceration associated with H.pylori?

A

Increased gastric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are complications of peptic ulceration?

A

Bleeding (acute-haemorrhage, chronic-anaemia)
Perforation (peritonitis)
Healing by fibrosis (obstruction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is metaplasia?

A

Transformation of normal tissue type into another normal cell (is reversible)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the histology change of Barrett’s oesophagus?

A

Squamous epithelium replaced with glandular epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Why might obesity be a cause of oesophageal reflux?

A

Increased intra-abdominal pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the second commonest cancer of the alimentary tract?

A

Stomach cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What can be associated with previous H.pylori infection?

A

Stomach cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the histology of stomach cancer?

A

Adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the spread of stomach cancer?

A

Direct - to surrounding structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the lymphatic spread of stomach cancer?

A

To regional lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the blood spread of stomach cancer?

A

Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the transcoelomic spread of stomach cancer?

A

Spread within peritoneal cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the prognosis for stomach cancer?

A

Very poor - 5 year survival rate <20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is dyspepsia?

A

Group of symptoms: pain or discomfort in upper abdomen, retrosternal pain, anorexia, nausea, vomiting, bloating, fullness, early satiety, heartburn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

When do you refer someone to endoscopy? (mnemonic)

A 
ALARMS or >55yo
A - anorexia
L - loss of weight
A - anaemia
R - recent onset of progressive symptoms
M - melaena/haematemesis or mass
S - swallowing problems (dysphagia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Patient presents with dyspepsia, what do you do first?

A

History and examination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Patient presents with dyspepsia, what bloods do you order?

A

FBC, ferritin, LFTs, U+Es, calcium, glucose, coeliac serology/serum IgA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Patient presents with dyspepsia, what drugs in drug history are important?

A

NSAIDs, steroids, bisphosphonates, Ca antagonists, nitrates, theophyllines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

If the patient is <55 and is positive for H.pylori, what is the next step?

A

Eradication therapy & symptomatic treatment with PPIs or H2R antagonists & lifestyle factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Is H.pylori gram negative or gram positive?

A

Gram negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Where does H.pylori colonise?

A

Gastric type mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Where does H.pylori reside?

A

Resides in the surface mucous layer and does not penetrate the epithelial layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the possible clinical outcomes of H.pylori infections?

A

Gastritis, chronic atrophic gastritis, intestinal metaplasia, gastric or duodenal ulcer, gastric cancer or MALT lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the possible consquences of antral predominant gastritis?

A

Increased acid production -> low risk stomach cancer, increased risk duodenal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are the possible consequences of mild mixed gastritis (in both antrum and body)?

A

Normal acid -> no significant disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are the possible consequences of corpus (body) predominant gastritis?

A

Decreased acid -> gastric atrophy, gastric cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are non-invasive diagnostic tests for H.pylori?

A

Serology (IgG against H.pylori), urea breath test, stool antigen test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are invasive diagnostic tests for H.pylori?

A

Endoscopy, biopsy, rapid slide urease test (CLOtest)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Why a rapid slide urease test (CLOtest) to test for H.pylori?

A

H.pylori secretes the urease enzyme which catalyses the conversion of urea to ammonia and carbon dioxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the majority of peptic ulcers caused by?

A

H.pylori infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are more common: duodenal ulcers or peptic ulcers?

A

Duodenal ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the symptoms of a peptic ulcer?

A

Epigastric pain/tenderness, nocturnal/hunger pain (more DU), back pain, N&V, weight loss, anorexia, haematemesis, meleana, anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Why might a patient with a peptic ulcer have back pain?

A

May be penetration of posterior DU

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

If a peptic ulcer bleeds, how may the patient present?

A

Haematemesis and/or melaena, or anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How are ulcers caused by H.pylori treated?

A

Triple therapy eradication therapy for 7 days to get rid of bacteria –> clarithromycin, amoxycillin and antacid medication e.g. proton pump inhibitors or H2 receptor antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is an example of a proton pump inhibitor used to treat peptic ulcers?

A

Omeprazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is an example of a H2 receptor antagonist used to treat peptic ulcers?

A

Ranitidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How many days triple therapy for H.pylori infection?

A

7 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are the complications of a peptic ulcer?

A

Acute bleeding, chronic bleeding, perforation, fibrotic stricture, gastric outlet obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the signs and symptoms of gastric outlet obstruction?

A

Vomiting (lacks bile/fermented foodstuff), early satiety, abdominal distention, weight loss, gastric splash, dehydration, loss of H+ and CL- in vomit, metabolic alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What would the blood results be for gastric outlet obstruction and what would the implications be?

A

Low Cl, low Na, low K

Renal impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

How would you diagnosis a gastric outlet obstruction?

A

UGIE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

How is a gastric outlet obstruction treated?

A

Endoscopic balloon dilation or surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

How do patients with gastric cancer present?

A

Dyspepsia, early satiety, N&V, weight loss, GI bleeding, iron deficiency anaemia, gastric outlet obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are the genes associated with heritable gastric cancer syndromes?

A

HDGC (autosomal dominant)

CDH-1 gene (E-cadherin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How do you manage a patient with gastric cancer?

A

Histological diagnosis - endoscopy and biopsy
Staging investigations - CT chest/abdo
MDT discussion
Treatment - surgical and chemo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What are the functions of the colon and rectum?

A

Fluid and electrolyte balance, waste management, continence, microbe related

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

The colon has more anaerobes than the small intestine: true or false?

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What do patients with colon or rectal problems complain of?

A

Change in bowel habit/continence, bleeding, pain, non-intestinal manifestations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is visceral pain?

A

Pain receptors in smooth muscle, afferent impulses running with sympathetic fibres, is poorly localised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Visceral pain is: well localised or poorly localised?

A

Poorly localised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What are the low risk features of rectal bleeding?

A

Transient symptoms (<6wks) of rectal bleeding with anal symptoms, patient is <40yo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What are the high risk features of rectal bleeding?

A

Persistent change in bowel habit (>6wks)
Persistent rectal bleeding without anal symptoms
Right sided abdominal mass
Palpable rectal mass
Unexplained iron deficiency anaemia
Patients in whom there is no clinical doubt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the protocol for managing patients who have low risk features for rectal bleeding?

A

Wait and watch (6wks):

Assessment and review, patient agreement, appropriate info/councelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is the protocol for managing patients who have high risk features for rectal bleeding?

A

Refer for visualisation of the large bowel:
Colonoscopy
Flexible/rigid sigmoidoscopy +/- barium enema
CT colongraphy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What are the investigations for CRC?

A

Endoscopy, colonscopy, biopsy, contrast imaging (barium enema), CT/CT colonography, MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is important for success of bowel anastomosis?

A

Tension free, well perfused, well oxygenated, clean surgical site, acceptable systemic state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What is faecal diversion?

A

Creation of an ileostomy or colostomy - a new path for waste material to leave the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What are some complications of bowel surgery?

A 
Anaesthetic related
Bleeding
Sepsis
VTE
Anastomotic breakdown
Small bowel obstruction
Would hernia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What are the symptoms of oesophageal disease?

A 
Heartburn
Retrosternal discomfort or burning
Waterbrash
Cough
Dysphagia
Odynophagia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is water brash?

A

Acid mixes with the excess saliva during reflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What are some of the causes of oesophageal dysphagia?

A 
Benign stricture
Malignant stricture
Eosinophilic oesophagitis
Motility disorders e.g. achalasia, presbyoesophagus
Extrinsic compression e.g. lung cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What are some investigations for oesophageal disease?

A 
Endoscopy:
Oesophago-gastro-duodenoscopy (OGD)
Upper GI endoscopy (UGIE)
Barium swallow (contrast radiography)
Oesophageal pH and manometry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What does hypermotility of the oesophagus look like on a barium swallow?

A

Corkscrew appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What are the symptoms of hypermotility of the oesophagus?

A

Severe, episodic chest pain +/- dysphagia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What is the treatment for hypermotility of the oesophagus?

A

Smooth muscle relaxants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What does manometry investigation show for hypermotility of the oesophagus?

A

Exaggerated, uncoordinated, hypertonic contractions of the oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What is hypomotility of the oesophagus associated with?

A

Connective tissue disease, diabetes, neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What causes hypomotility of the oesophagus?

A

Failure of LOS mechanism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What causes achalasia?

A

Functional loss of myenteric plexus ganglion cells in the distal oesophagus and LOS = failure of LOS to relax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What are the functional consequences of achalasia?

A

Failure of LOS to relax = distal obstruction of the oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What are the symptoms of achalasia?

A

Progressive dysphagia, weightless, chest pain, regurgitation and chest infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What is the treatment for achalasia?

A

Pharmacological: nitrates, Ca+ channel blockers,
Endoscopic: botox, pneumatic balloon dilation
Radiological: pneumatic balloon dilation
Surgical: myotomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What are the complications of achalasia?

A

Pneumonia, lung disease, increased risk of squamous cell oesophageal carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Which can lead to GORD: hypermotility or hypomotility?

A

Hypomotility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What are some of the causes of GORD?

A

Pregnancy, smoking, obesity, alcoholism, hypomotility, drugs lowering LOS pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What are some of the symptoms of GORD?

A

Heartburn, sleeping disturbance, water brash, cough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is GORD pathologically?

A

Acid (and bile) exposure in the lower oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

When should endoscopy be performed for GORD?

A

In presence of ALARM features for malignancy e.g. vomiting, dysphagia, weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What are some of the causes of GORD without abnormal anatomy?

A 
Increased transient relaxation of LOS
Hypotensive LOS
Delayed gastric emptying
Delayed oesophageal emptying
Decreased oesophageal acid clearance
Decreased tissue resistance to acid/bile
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What are the two main types of hiatus hernia?

A

Sliding

Para-oesophageal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What predisposes a person to a hiatus hernia?

A

Age (>50)

Obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What are some of the complications of GORD?

A

Stricure
Ulceration
Glandular metaplasia (Barrett’s oesophagus)
Carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What are the treatments for Barrett’s oesophagus?

A

Endoscopic mucosal resection (EMR)
Radio-frequency ablation (RFA)
Oesophagectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What are the treatment options for GORD?

A

Lifestyle measures
Pharmacological: Alginates (Gaviscon), H2RA (Ranitidine), PPI (Omeprazole, Lansoprazole)
Anti-reflux surgery: fundoplication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What are some of the symptoms of oesophageal cancer?

A

Progressive dysphagia, weight loss and anorexia, odynophagia, chest pain, cough, haematemesis (vomiting blood), pneumonia, vocal cord paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Which oesophageal cancer type most commonly affects the distal oesophagus?

A

Adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Which oesophageal cancer type most commonly affects the proximal and middle 1/3 of the oesophagus?

A

Squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What are the common metastases for oesophageal cancer?

A

Liver, bone, brain, lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What are the investigations for oesophageal cancer?

A

Endoscopy, biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What are the staging investigations for oesophageal cancer?

A

CT scan
Endoscopic ultrasound
PET scan
Bone scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What are the treatment options for oesophageal cancer?

A

Only potential cure: surgical oesophagectomy +/- adjuvant or neoadjuvant chemotherapy
Combined chemo and radiotherapy for longer term survival
Symptom palliation: endoscopic (stent, PEG), chemotherapy, radiotherapy, brachytherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What is eosinophilic oesophagitis?

A

A chronic, allergic inflammatory disease of the oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What is the cause of eosinophilic oesophagitis?

A

Eosinophil (WBC) infiltration into the epithelial lining of the oesophagus and initiates and inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What are the symptoms of eosinophilic oesophagitis?

A

Dysphagia and food bolus obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What are the treatment options for eosinophilic oesophagitis?

A

Topical/swallowed corticosteroids
Dietary elimination - if allergen suspected
Endoscopic dilatation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What is the investigation to work out the T/N stage for oesophageal cancer?

A

Endoscopic ultrasound (EUS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What is the investigation to work out the M stage for oesophageal cancer?

A

PET CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

What conduits can be used for an oesophagectomy?

A

Stomach or colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What are the modifiable risk factors for stomach cancer?

A

Alcohol, smoking, infection with h.pylori virus, excessive consumption of salted fish, pickled vegetables and cured meats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What are the investigations for stomach cancer?

A

Endoscopy

Constrast meal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

What are the staging investigations for stomach cancer?

A

CT chest/abdomen, laparoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What are the possible surgeries for gastric cancer?

A

Subtotal gastrectomy

Total gastrectomy and Roux en Y reconstruction (oesophago-jejunostomy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What are the two options for operating for gastrectomy?

A

Laparoscopic distal gastrectomy

Open gastrectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What is pancolitis?

A

A form of ulcerative colitis which affects the entire large bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

What are the two main diseases of inflammatory bowel disease?

A

Ulcerative colitis

Crohn’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Where does ulcerative colitis affect?

A

Large bowel only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

How does ulcerative colitis usually spread?

A

Rectum to proximal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What are some of the histological features of ulcerative colitis?

A 
No granulomas!
Mucosa inflammation
Cryptitis
Crypt abscesses
Mucosal atrophy
Ulceration
Submucosal fibrosis
Limited mainly to mucosa and submucosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

What is reactive atypia?

A

Changes due to inflammation or injury without neoplastic change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

What type of UC becomes a risk for developing cancer?

A

Pancolitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

What are other complications of UC?

A

Haemorrhage
Perforation
Toxic dilatation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Does Crohn’s affect more females or males?

A

Females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Where does Crohn’s disease affect?

A

Any level of GIT from mouth to anus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

When are the peaks of age for Crohn’s disease?

A

20-30yrs

60-70yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

What ethnic populations are most affected by Crohn’s disease?

A

Caucasians and Jewish populations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Where does Crohn’s mostly affect?

A

Small intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

What are some pathological features of Crohn’s disease?

A

Wall thick
Narrowing of lumen
Skip lesions
Cobblestone appearance - ulcerations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

What causes skip lesions in Crohn’s disease?

A

Sharp demarcation between diseased segments and adjacent normal tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

What are some of the histological features of Crohn’s disease?

A 
Non-caseating granulomas!
Cryptitis and crypt abscesses
Ulceration - deep
Transmural inflammation - chain of pearls
Fibrosis
Paneth cell metaplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

Which has non-caveating granulomas on histological examination: ulcerative colitis or Crohn’s disease?

A

Crohn’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

What are the long term pathological features of Crohn’s disease?

A 
Malabsorption
Strictures
Fistulas and abscesses
Perforation
Increased risk of cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Which has transmural inflammation: ulcerative colitis or Crohn’s disease?

A

Crohn’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

Which has inflammation which is limited to the mucosa: ulcerative colitis or Crohn’s disease?

A

Ulcerative colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

Which has granulomas: ulcerative colitis or Crohn’s disease?

A

Crohn’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

How does ischaemic enteritis occur?

A

Acute occlusion of 1 of the 3 major supply vessels to the bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

What some predisposing conditions for ischaemic enteritis?

A

Arterial thrombosis: atherolsclerosis, vasculitis, dissecting aneurysm, oral contraceptives
Arterial embolism: cholesterol embolism, acute atheroembolism
Non-occlusive ischaemia: cardiac failure, shock/dehydration, vasoconstrictive drugs (propranolol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Where in the colon is vulnerable to acute ischaemia?

A

Splenic flexure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

What are some of the histological features of acute ischaemia?

A 
Oedema
Interstitial haemorrhages
Sloughing necrosis of mucosa = ghost outlines
Nuclei indistinct
Vascular dilation
Initial absence of inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

What are some of the features of chronic ischaemia of the bowel?

A 
Mucosal inflammation
Ulceration
Submucosal inflammation
Fibrosis
Stricture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

What is radiation colitis?

A

Abdominal irradiation can impair the normal proliferative activity of the small and large bowel epithelium

162
Q

What are the symptoms of radiation colitis?

A

Anorexia, abdominal cramps, diarrhoea, malabsorption

163
Q

Which type of radiation is most likely to result in radiation colitis?

A

Rectum-pelvic radiotherapy

164
Q

What are some of the histological features of radiation colitis?

A 
Bizarre cellular changes
Inflammation - crypt abscesses and eosinophils
Ulceration
Necrosis
Haemorrhage
Perforation
165
Q

How long is the average appendix?

A

6-7cm

166
Q

What happens in appendicitis?

A

Acute inflammation

167
Q

What are some of the histological features of appendicitis?

A

Macro: exudate, perforation, abscess
Micro: acute suppurative inflammation in wall and pus in lumen, acute gangrenous full thickness necrosis +/- perforation

168
Q

What are the two subtypes of dysplasia?

A

Low grade

High grade

169
Q

What are three types of adenoma?

A

Tubular
Villous
Tubulovillous

170
Q

How would low grade dysplasia be described histologically?

A

Increased nuclear numbers
Increased nuclear size
Reduced mucin

171
Q

How would high grade dysplasia be described histologically?

A

Carcinoma in situ
Crowded
Very irregular
Not yet invasive

172
Q

What type of cancer/dysplasia are most colorectal carcinomas?

A

Adenocarcinoma

173
Q

What are some risk factors for colorectal carcinoma?

A

Lifestyle
FH
IBD - UC and Crohn’s disease
Genetics - FAP, HNPCC

174
Q

What are the features of right-sided colorectal adenocarcinoma?

A 
Exophytic/polypoid
Anaemia
Vague pain
Weakness
Obstruction
175
Q

What are the features of left-sided colorectal adenocarcinoma?

A

Annular - napkin ring lesion
Bleeding
Altered bowel habit
Obstruction

176
Q

Where does upper GI bleeding occur?

A

From oesophagus, stomach or duodenum

Proximal to ligament of Trietz

177
Q

Where does lower GI bleeding occur?

A

Distal to duodenum (jejunum, ileum, colon)

Distal to ligament of Trietz

178
Q

What is the landmark us to separate lower and upper GI bleeding?

A

Ligament of Trietz

179
Q

What could present as upper GI bleeding?

A

Haematemesis

Melaena

180
Q

What marker could indicate upper GI bleeding?

A

Elevated urea (digested blood: haem->urea)

181
Q

What symptoms is upper GI bleeding associated with?

A

Dyspepsia, reflux, epigastric pain

182
Q

Which class of drugs may cause upper GI bleeding?

A

NSAIDs

183
Q

What are signs of lower GI bleeding?

A

Fresh blood/clots, magenta stools

184
Q

What symptoms are lower GI bleeding associated with?

A

Typically painless

185
Q

What will the urea levels be like for lower GI bleeding?

A

Normal urea (rarely elevated if proximal small bowel origin)

186
Q

What is melena?

A

Dark black, tarry faeces associated with upper GI bleeding

187
Q

53yo male reports passing black, loose, sticky bowel motions for preceding 24hrs. What might be the cause?

A

Upper GI bleeding

188
Q

What are some causes of oesophageal bleeding?

A 
Oesophageal ulcer
Oesophagitis
Oesophageal varices
Mallory Weiss tear
Oesophageal malignancy
189
Q

What are some causes of gastric bleeding?

A 
Gastric ulcer
Gastritis
Gastric varices
Portal hypertensive gastropathy
Gastric malignancy
Dieulafoy's lesion
Angiodysplasia
190
Q

What are some causes of duodenal bleeding?

A

Duodenal ulcer
Duodenitis
Angiodysplasia

191
Q

What is a Mallory Weiss tear?

A

Bleeding from a laceration in the mucosa at the junction of the stomach and oesophagus

192
Q

What is dieulofoy’s lesion?

A

Large tortuous arteriole (most commonly in stomach wall) which erodes and bleeds

193
Q

What usually causes a Mallory Weiss tear?

A

Severe vomiting e.g. alcoholism, bulimia

194
Q

What are two damaging forces to gastric mucosa?

A

Gastric acidity

Peptic enzymes

195
Q

What substances can injure the gastric mucosa?

A 
H. pylori infection
NSAIDs
Aspirin
Smoking
Alochol
Gastric hyperacidity
Duodenal-gastric reflux
196
Q

What can lead to peptic ulceration?

A 
Increasing damaging substances
Impaired defences (damaged gastric mucosa)
197
Q

Which are the most common: gastric ulcers or duodenal ulcers?

A

Duodenal ulcers

198
Q

What are the risk factors for peptic ulcers?

A

H.pylori
NSAIDs/aspirin
Alcohol excess
Systemic illness = stress ulcers

199
Q

How is H.pylori a risk factor for peptic ulcers?

A

Produces urease -> ammonia produced -> buffers gastric acid locally = increased acid production

200
Q

How do NSAIDs/aspirin cause peptic ulcers?

A

Prostaglandin production -> reduced mucus and bicarbonate excretion -> reduced physical defences

201
Q

Where might be a hidden place to find a gastric carcinoma?

A

Under a gastric ulcer

202
Q

What causes recurrent poor healing duodenal ulcers?

A

Zollinger-Ellison syndrome

203
Q

What is Zollinger-Ellison syndrome?

A

A gastrin-secreting pancreatic tumour

204
Q

What does Zollinger-Ellison syndrome result in?

A

Overproduction of gastrin which causes ulcers

205
Q

When might gastritis or duodentitis cause bleeding?

A

Impaired coagulation causes by:
Medical conditions
Anti-coagulants
Anti-platelets

206
Q

When might oesophagitis cause bleeding?

A 
Reflux oseophagitis
Hiatus hernia
Alcohol
Biphosphonates
Systemic illness
207
Q

What are examples of anti-platelets that are likely to cause upper GI bleeding?

A

Clopidogrel

Ticagrelor

208
Q

What are examples of anti-coagulants that are likely to cause upper GI bleeding?

A

Warfarin
Rivaroxaban
Apixaban
Dabigatran

209
Q

An injecting drug user presents to A+E with fresh haematemesis and collapse. On examination you notice a mass in his left upper quadrant. What is the most likely diagnosis?

A

Liver cirrhosis (secondary to chronic hep C)

210
Q

An injecting drug user presents to A+E with fresh haematemesis and collapse. On examination you notice a mass in his left upper quadrant. What is the most likely cause of the LUQ mass?

A

Enlarged spleen due to portal hypertension

Portal hypertension is cause of varies which have cause haematemesis

211
Q

What are varices usually due to?

A

Secondary to portal hypertension (due to liver cirrhosis)

212
Q

What are the most common type of varices?

A

Oesophageal

213
Q

What malignancies might you think of for upper GI bleeding?

A

Oesophageal cancer

Gastric cancer

214
Q

What is angiodysplasia?

A

Vascular malformation which can occur anywhere in the GIT

215
Q

What is angiodysplasia often associated with?

A

Chronic conditions including heart valve replacement

216
Q

For GI bleeding, when should UGIE be performed?

A

Within 24hrs, sooner if unstable

217
Q

24you female, constipation, presenting with 24hr history of painless fresh red bleeding per rectum which occurred following a period of straining. What is the diagnosis?

A

Haemorrhoids

218
Q

What are some colonic causes of lower GI bleeding?

A 
Diverticular disease
Haemorrhoids
Vascular malformations (angiodysplasia)
Neoplasia (carcinoma or polyps)
Ischaemic colitis
Radiation enteropathy/proctitis
IBD
219
Q

What are the lower GI bleeding diagnostic investigations?

A

Flexible sigmoidoscopy
Full colonoscopy
CT angiography

220
Q

What is diverticular disease?

A

Protrusion of the inner mucosal lining through the outer muscular layer forming a pouch

221
Q

What is the difference between diverticulosis and diverticulitis?

A 
Diverticulosis = presence of pouches
Diverticulitis = inflammation of pouches
222
Q

What are haemorrhoids?

A

Enlarged vascular cushions around anal canal

223
Q

What are haemorrhoids associated with?

A

Straining
Constipation
Low fibre diet

224
Q

What is the treatment of haemorrhoids?

A

Elective surgical intervention

225
Q

How is angiodysplasia treated?

A

Argon phototherapy

Medication incl. tranexamic acid, thalidomide

226
Q

What symptoms does ischaemic colitis present with?

A

Crampy abdominal pain and sudden bleeding

227
Q

What are complications of ischaemic colitis?

A

Gangrene and perforation

228
Q

What might someone have a PMH of if they have radiation proctitis?

A

Radiotherapy - cervical/prostate

229
Q

What is the treatment for radiation proctitis?

A

Argon plasma coagulation (APC)
Sulcrafate enemas
Hyperbaric oxygen

230
Q

What are small bowel causes of acute lower GI bleeding?

A

Meckel’s diverticulum
Small bowel angiodysplasia
Small bowel tumour/GIST (gastro-intestinal stromal tumour)
Small bowel ulceration
Aortoentero fistulation (following AAA repair)

231
Q

What are small bowel investigations for acute lower GI bleeding?

A

CT angiogram
Meckel’s scan (scintigraphy)
Capsule endoscopy
Double balloon enteroscopy

232
Q

What is Meckel’s diverticulum?

A

A true congenital diverticulum

Slight bulge in the small intestine and a remnant of the yolk sac

233
Q

What is the management of GI bleeding?

A

ABCDE
Circulation: IV fluids, blood transfusion if Hb<7g/dl, blood samples to lab
Catheter

234
Q

What is shock?

A

Circulatory collapse resulting in inadequate tissue oxygen delivery leading to global hypo perfusion and tissue hypoxia

235
Q

What are the signs for haemorrhagic shock?

A 
High RR (tachypnoea)
Rapid pulse (tachycardia)
Anxiety or confusion
Cool clammy skin
Low urine output (oliguria)
Low BP (hypotension)
236
Q

What are the two scoring systems used in risk stratification of UGIB?

A

Rockall Score

Blatchford Score

237
Q

In the Blatchford scoring system for UGIB, what factors are looked at for the pre-endoscopy score?

A

Blood urea
Haemoglobin
Systolic BP
Other markers: hepatic disease/cardiac failure

238
Q

What score in the Blatchford scoring system for UGIB is associated with a greater than 50% risk of needing an intervention?

A

> 6

239
Q

What are improved factors for patients who are admitted to dedicated GI bleeding units?

A 
Improved mortality
Improved outcome
Prompt resus
Close medical and surgical liaison
Protocolised care
240
Q

What is the management for peptic ulcers?

A

PPI
Endoscopy with endotherapy
Angiography with embolisation
Laparotomy

241
Q

What is the management of varices?

A 
Endotherapy:
Oesophageal - band ligation/glue injection
Gastric or rectal - glue injection
IV terlipressin
IV BS antiobiotics
Correct coagulopathy
242
Q

What does IV terlipressin due in varices treatment?

A

Vasoconstricts splanchnic blood supply and reduces blood flow to portal vein, reducing portal pressures

243
Q

Where do magenta stools typically come from?

A

Right colon or distal small bowel

244
Q

What is haemotochezia?

A

Passage of fresh or altered blood per rectum - may be upper or lower GI

245
Q

What is an acute abdomen?

A

A combination of signs and symptoms, including abdominal pain, which results in a patient being referred for an urgent general surgical opinion

246
Q

What three things to consider for an acute abdomen diagnosis?

A

Peritonitis
Intestinal obstruction
Abdominal pain

247
Q

What are the routes of infection for peritonitis?

A

Perforation of GI/biliary tract
Female genital tract
Abdominal wall penetration
Haemotogenous spread

248
Q

What are the bacteria in the upper GI tract normally?

A

Aerobes

249
Q

What are the bacteria in the lower GI tract normally?

A

Anaerobes

250
Q

What is the main bacteria in the peritoneum normally?

A

Aerobes

251
Q

What are the cardinal features of intestinal obstruction?

A 
Pain
Vomiting
Distention
Constipation
Borborygmi
252
Q

What is borborygmi?

A

A rumbling or gurgling noise made by the movement of fluid and gas in the intestine

253
Q

What do the features of intestinal obstruction depend on?

A

Site of blockage - distal or proximal

254
Q

What are the three main character types of pain?

A

Visceral - diffuse, difficult to localise, internal organs e.g. deep, squeezing, dull
Somatic - located in skin/deep tissues, well localised e.g. aching, throbbing
Referred - pain perceived at a location other than the site of the painful stimulus

255
Q

Where are the pain receptors for visceral pain?

A

In smooth muscle

256
Q

How do the afferent impulses run for visceral pain?

A

With sympathetic fibres accompanying segmental vessels e.g. CP, SMA, IMA

257
Q

Where are the pain receptors for somatic and referred pain?

A

In parietal peritoneum or abdominal wall

258
Q

How do the afferent impulses run for somatic and referred pain?

A

With segmental nerves

259
Q

What are the effects of peritonitis and intestinal obstruction?

A

Fluid loss, sepsis -> circulatory collapse -> death

260
Q

What would the patient be like if they had peritonitis pain?

A

Lying still, sore to move

261
Q

What would a patient be like if they had body wall pain?

A

Sore to touch

262
Q

What would a patient be like if they had colic pain?

A

Look like ‘a woman in childbirth’

263
Q

What is the management procedure for an acute abdomen?

A

Assess (+ resuscitate)
Investigate
Observe
Treat

264
Q

In your assessment of an acute abdomen, what questions should you ask?

A

What is the problem?
What are its effects?
What should I do?

265
Q

What investigations would you do for an acute abdomen?

A

Ward: urine
Lab: FBC, U+E, LFT
Radiology: Plain XR, US, axial CT

266
Q

What are you trying to do when resuscitating an acute abdomen?

A 
Restore circulating fluid volume
Ensure tissue perforation
Enhance tissue oxygenation
Treat sepsis
Decompress gut
Ensure adequate pain relief
267
Q

What are the general treatments for an acute abdomen?

A

Pain relief
Antibiotics
Definitive intervention e.g. surgery

268
Q

What are the five main types of viral hepatitis?

A

A, B, C, D + E

269
Q

Which of the hepatitic viruses are enteric?

A

A+E

270
Q

Which of hepatitic viruses are parenteral?

A

B,C+D

271
Q

Which of the hepatitic viruses are self-limiting acute infections?

A

A+E

272
Q

Which of the hepatitic viruses are chronic diseases?

A

B,C+D

273
Q

Which immunoglobulin increases with hepatitis A?

A

IgG

274
Q

Which immunoglobulin increases with acute infection with hepatitis A?

A

IgM

275
Q

Which enzyme is elevated in hepatitis A?

A

ALT

276
Q

What do patients with chronic hepatitis B have a risk of developing?

A

Cirrhosis of the liver

277
Q

What do patients with cirrhosis of the liver have a risk of developing?

A

HCC (hepatocellular carcinoma)

ESLD (end stage liver disease)

278
Q

What are the treatment options for HBV?

A

Antiviral drugs
Pegylated inferon
Treatment of symptoms

279
Q

What are examples of antiviral drugs used for treatment of HBV?

A

Lamiduvine
Entecavir
Adefovir

280
Q

What is the usual transmission of HCV?

A

Blood

Mother to child (vertical transmission)

281
Q

What is the main treatment used nowadays for HCV?

A

Direct-acting antivirals (DAA)

282
Q

Which hepatitis infection is very resistant to treatment?

A

Hepatitis D virus

283
Q

What is the commonest hepatitis virus to cause acute hepatitis in Grampian?

A

Hepatitis E

284
Q

What is the treatment for hepatitis E?

A

No specific treatment, self-limiting

285
Q

What does non-alcoholic fatty liver disease (NAFLD) encompass?

A

Simple steatosis
Non alcoholic steatohepatitis
Fibrosis and cirrhosis

286
Q

What conditions is NAFLD associated with?

A

Diabetes mellitus
Obesity
Hypertriglyceridemia
Hypertension

287
Q

What are the risk factors for NAFLD?

A

Conditions associated e.g. DM, HT, obesity
Age
Ethnicity (Hispanics)
Genetic factors

288
Q

What is the natural history of progression for NAFLD?

A

Normal liver -> steatosis -> NASH +/- fibrosis -> cirrhosis

289
Q

What does NASH stand for?

A

Non-alcoholic steatohepatitis

290
Q

What diagnostic tests are there for NAFLD?

A 
Biochemical tests: AST/ALT ratio
Enhanced liver fibrosis (ELF) panel
Cytokeratin-18
Ultrasound
Fibroscan
MRI/CT
MR spectroscopy
Liver biopsy
291
Q

What does the NAFLD score do?

A

Estimates amount of scarring to liver to evaluate progression/stabilisation

292
Q

What are the treatment options for NAFLD?

A

Diet and weight reduction
Exercise
Weight reduction surgeries
Insulin sensitizers e.g. Metformin, Pioglitazone
Glucagon-peptide-1 (GLP-1) analogues e.g. Liraglutide
Farnesoid X nuclear receptor ligand e.g. Obeticholic acid
Vitamin E

293
Q

What are some examples of autoimmune liver disease?

A

Autoimmune hepatitis
Primary biliary cholangitis (PBS)
Primary sclerosing cholangitis (PSC)

294
Q

Which autoimmune liver diseases are female predominant?

A

Autoimune hepatitis

PBC

295
Q

Which autoimmune liver disease is male predominant?

A

PSC

296
Q

Who qualifies for a liver transplant?

A

Chronic liver disease with poor predicted survival
Chronic liver disease with associated poor quality of life
HCC
Acute liver failure
Genetic diseases e.g. primary oxaluria, tyrosemia

297
Q

What are some contraindications for a liver transplant?

A

Active extra hepatic malignancy
Hepatic malignancy with microvascular or diffuse tumour invasion
Active substance or alcohol abuse
Active and uncontrolled infection outside of hepatobiliary system
Severe cardiopulmonary or other comorbid condition
Psychosocial problems that would preclude recovery
Brain death

298
Q

What scoring systems are used to prioritise cirrhosis?

A

Child’s Pugh scoring A, B and C
MELD score (bilirubin, creatinine and INR)
UKELD (bilirubin, sodium, creatinine and INR)

299
Q

What can liver failure be a result of?

A

Acute liver injury

Chronic liver injury e.g. cirrhosis

300
Q

What can acute liver injury be a result of?

A

Hepatitis - viruses, alcohol, drugs

Bile duct obstruction

301
Q

What is the pathology of viral hepatitis?

A

Inflammation of the liver

Liver cell damage and death of individual liver cells

302
Q

What happens in alcoholic liver disease?

A

Response of liver to excess alcohol
Fatty change and alcoholic hepatitis: acute inflammation -> liver cell death -> liver failure
Progress to cirrhosis

303
Q

What is jaundice caused by?

A

Increased levels of circulating bilirubin caused by altered metabolism of bilirubin

304
Q

What is pathway of bilirubin metabolism?

A

Pre-hepatic: breakdown of haemoglobin in spleen to haem and globin, haem is converted to bilirubin, release of bilirubin into circulation
Hepatic: uptake of bilirubin by hepatocytes, conjugation of bilirubin in hepatocytes, excretion of conjugated bilirubin into biliary system
Post-hepatic: transport of conjugated bilirubin in biliary system, breakdown of bilirubin conjugate in intestine, re-absorption of bilirubin

305
Q

What are the three classifications of jaundice?

A

Pre-hepatic
Hepatic
Post-hepatic

306
Q

What are the causes of pre-hepatic jaundice?

A

Increased release of haemoglobin from red cells + therefore increased quantity of bilirubin (haemolysis)
Impaired transport

307
Q

What are the hepatic causes of jaundice?

A

Cholestasis - reduction/stoppage of bile flow

Intra-hepatic bile duct obstruction

308
Q

What is cholestasis?

A

A reduction or stoppage of bile flow resulting in an accumulation of bile within hepatocytes or bile canaliculi

309
Q

What are some causes of cholestasis?

A

Viral hepatitis
Alcoholic hepatitis
Liver failure
Drugs: therapeutic or recreational

310
Q

What is meant by predictable vs unpredictable drug-induced cholestasis?

A 
Predictable = dose related
Unpredictable = not dose related
311
Q

What are some causes of intra-hepatic bile duct obstruction?

A

Primary biliary cholangitis (PBC)
Primary sclerosing cholangitis (PSC)
Tumours of the liver e.g. HCC, tumours of intra-hepatic bile ducts, metastatic tumours

312
Q

What is cholangiocarcinoma?

A

Malignant tumour of bile duct epithelium

313
Q

What is the pathology of primary biliary cholangitis?

A

Granulomatous inflammation involving bile ducts, loss of intra-hepatic bile ducts, progression to cirrhosis

314
Q

What is the pathology of primary sclerosing cholangitis?

A

Chronic inflammation and fibrous obliteration of bile ducts, loss of intra-hepatic bile ducts

315
Q

What disease is primary sclerosing cholangitis often associated with?

A

Inflammatory bowel disease (IBD)

316
Q

What are you of increased risk of with primary sclerosing cholangitis?

A

Cholangiocarcinoma

317
Q

What are some of the causes of cirrhosis?

A 
Alcohol
Hepatitis B/C
Immune mediated liver disease
Metabolic disorders e.g. excess iron or copper
Obesity
Cryptogenic
318
Q

What is the pathology of cirrhosis?

A

Diffuse process involving whole liver, loss of liver structure as replaced by nodules of hepatocytes and fibrous tissue

319
Q

What are some complications of liver cirrhosis?

A

Altered liver function - failure
Abnormal blood flow - portal hypertension
Increased risk of HCC

320
Q

What are some of the causes of post-hepatic jaundice?

A

Cholelithiasis
Diseases of gall bladder
Extra-hepatic duct obstruction - defective transport of bilirubin by biliary ducts

321
Q

What are the risk factors for gallstones?

A

Obesity, diabetes

322
Q

What are some diseases of the gall bladder that can cause post-hepatic jaundice?

A

Inflammation e.g. acute or chronic cholecystitis

323
Q

What is acute cholecystitis?

A

Acute inflammation of the gall bladder

324
Q

What are some complications of acute cholecystitis?

A

Empyema - perforation of the gall bladder or biliary peritonitis

325
Q

What is chronic cholecystitis?

A

Chronic inflammation and fibrosis of the gall bladder

326
Q

What are some causes of common bile duct obstruction?

A

Gallstones
Bile duct tumours
Benign stricture
External compression e.g. tumours

327
Q

What are the effects of common bile duct obstruction?

A

Jaundice
No bile excreted into duodenum
Infection of bile proximal to obstruction - ascending cholangitis
Secondary biliary cirrhosis if obstruction prolonged

328
Q

What are the detoxification functions of the liver?

A

Urea produced from ammonia
Detoxification of drugs
Bilirubin metabolism
Breakdown of insulin and hormones

329
Q

What are the immune functions of the liver?

A

Combating infections
Clearing the blood of particles and infections, including bacteria
Neutralising and destroying all drugs and toxins

330
Q

What are the storage functions of the liver?

A

Stores glycogen
Stores vitamin A, D, B12 and K
Stores copper and iron

331
Q

What is bilirubin a product of?

A

Haem metabolism

332
Q

What is bilirubin initially bound to in its unconjugated form?

A

Albumin

333
Q

What is bilirubin pre-hepatically elevated due to?

A

Haemolysis

334
Q

What is bilirubin hepatically elevated due to?

A

Parenchymal damage

335
Q

What is bilirubin post-hepatically elevated due to?

A

Obstruction

336
Q

What are aminotransferases and where are they found?

A

Enzymes present in hepatocytes

337
Q

Which is more specific ALT or AST?

A

ALT

338
Q

What does ALT stand for?

A

Alanine transaminase

339
Q

What does AST stand for?

A

Aspartate transaminase

340
Q

What does an AST/ALT ratio greater than 2:1 point towards?

A

Alcoholic liver disease (ALD)

341
Q

What is alkaline phosphatase and where is it found?

A

Enzymes present in bile ducts

342
Q

When is alkaline phosphatase (ALP) elevated?

A

With obstruction or liver infiltration

343
Q

Where is alkaline phosphatase (ALP) also found?

A

Bone, placenta, intestines

344
Q

What is gamma GT?

A

Non specific liver enzyme

345
Q

When is gamma GT elevated?

A

Alcohol use

346
Q

What is gamma GT used for?

A

To confirm source of ALP

347
Q

What else can raise gamma GT levels?

A

Drugs e.g. NSAIDs

348
Q

What is albumin an important test for?

A

Synthetic function of the liver

349
Q

What do low levels of albumin suggest?

A

Chronic liver disease

350
Q

What can albumin also be low in (apart from chronic liver disease)?

A

Kidneys disorders, malnutrition

351
Q

What does prothrombin time (PT) indict?

A

Degree of liver dysfunction

352
Q

What is prothrombin time used to calculate?

A

Scores to decide stage of liver disease/who needs liver transplant/who gets liver transplant

353
Q

What does creatinine test?

A

Kidney function

354
Q

What is platelet count an indirect marker of?

A

Portal hypertension

355
Q

Why is platelet count low in cirrhotic subjects?

A

Cirrhosis results in splenomegaly (hypersplenism)

356
Q

What does splenomegaly and caput medusae suggest?

A

Portal hypertension

357
Q

At was plasma bilirubin level is jaundice detectable?

A

Over 34μmol/L

358
Q

Which classification of jaundice is conjugated?

A

Pre-hepatic

359
Q

Which classification of jaundice is unconjugated?

A

Hepatic and post-hepatic

360
Q

What are clues on history of pre-hepatic jaundice?

A

Fatigue, dysponea, chest pain, history of anaemia, acholuric jaundice

361
Q

What are the clues on history of hepatic jaundice?

A

Risk factors for liver disease e.g. IVDU, drug intake

Decompensation (ascites, varicella bleed, encephalopathy)

362
Q

What are the clues on history of post-hepatic jaundice?

A

Abdominal pain

Cholestasis (pruritus, pale stools, high coloured urine)

363
Q

What are the clues on clinical examination of pre-hepatic jaundice?

A

Pallor, splenomegaly

364
Q

What are the clues on clinical examination of hepatic jaundice?

A

Stigmata of CLD (spider naevi, gynaecomastia)
Ascites
Asterixis - liver flap

365
Q

What are the clues on clinical examination of post-hepatic jaundice?

A

Palpable gall bladder (Courvoisier’s sign)

366
Q

What are the investigations after diagnosis of jaundice?

A

Liver screen: hep B+C serology, autoantibody profile, serum immunoglobulins, ceruloplasmin and copper, ferritin and transferrin saturation, alpha-1 anti-tyrpsin, fasting glucose and lipid profile
US of abdomen

367
Q

What is ERCP?

A

Endoscopic retrograde cholangio-pancreatography

368
Q

What is MRCP?

A

Magnetic resonance cholangio-pancreatography

369
Q

What are the complications of ERCP?

A

Sedation required
Pancreatitis
Cholangitis
Sphincterotomy - bleeding/perforation

370
Q

What is PTC imaging modality?

A

Percutaenous transhepatic cholangiogram (PTC)

371
Q

What is endoscopic ultrasound (EUS) used for?

A

Characterising pancreatic masses
Staging of tumours
Fine need aspirate (FNA) of tumours and cysts
Excluding biliary microcalculi

372
Q

How long does liver disease last before it is chronic?

A

6 months

373
Q

What does physical examination reveal if ascites?

A

Dullness in flanks and shifting dullness

374
Q

What is the corroborating evidence on examination for ascites?

A

Spider naevi, palmar erythema, abdominal veins, fetor hepaticus
Umbilical nodule
JVP elevation
Flank haematoma

375
Q

What is measured in ascitic fluid on diagnostic paracentesis?

A

Protein and albumin concentration
Cell count and differential
SAAG (serum-ascites albumin gradient)

376
Q

What level of SAAG would indicate portal hypertension?

A

> 1.1g/dl

377
Q

What does high gradient SAAG indicate?

A

Portal hypertension

378
Q

What does low gradient SAAG indicate?

A 
Malignancy
TB
Chylous ascites
Pancreatitis
Biliary ascites
Nephrotic syndrome
Serositis
379
Q

Apart from portal hypertension, what could high gradient SAAG indicate?

A 
Chronic heart failure
Constrictive pericarditis
Budd Chiarri syndrome
Myxedema
Massive liver mets
380
Q

What are the treatment options for ascites?

A 
Diuretics
Large volume paracentesis
TIPS - transjugular intrahepatic portosystemic shunt
Aquaretics
Liver transplant
381
Q

What causes varices?

A

Portal hypertension

382
Q

Where do varices typically occur?

A 
Porto-systemic anastomoses:
Skin - caput medusae
Oesophageal and gastric
Rectal
Posterior abdominal wall
Stomal
383
Q

What is the management for varices?

A

Resuscitation
Good IV access
Blood transfusion as required
Emergency endoscopy

384
Q

What is hepatic encephalopathy?

A

Confusion or altered level of consciousness due to liver failure

385
Q

What clinical signs might indicate hepatic encephalopathy?

A

Liver flap and fetor hepaticus

386
Q

What are the investigations for HCC?

A

Tumour markers: AFP
Ultrasound
CT
MRI

387
Q

What scoring systems are used for alcohol screening tests?

A

FAST and AUDIT

388
Q

Regarding alcoholism, what does the acronym CAGE remind you to ask when doing a history?

A

Have you ever felt the need to CUT down?
Have you ever felt ANNOYED by criticism of your drinking?
Have you ever felt GUILTY about your drinking?
Do you need an EYEOPENER

389
Q

In the grading of hepatic encephalopathy what is 1?

A

Mild confusion

390
Q

In the grading of hepatic encephalopathy what is 4?

A

Coma

391
Q

What are the symptoms and signs of spontaneous bacterial peritonitis?

A

Abdominal pain, fever, rigors, renal impairment, signs of sepsis, tachycardia, pyrexia

392
Q

An ascitic tap for spontaneous bacterial peritonitis, what are you looking at?

A

Fluid protein and glucose levels
Cultures
White cell count

393
Q

What would the neutrophil count be above in spontaneous bacterial peritonitis?

A

> 0.25x10^9/L

394
Q

What would the protein be below in spontaneous bacterial peritonitis?

A

<25g/L

395
Q

What is the treatment for spontaneous bacterial peritonitis?

A

IV antibiotics
Ascitic fluid drainage
IV albumin infusion

396
Q

What investigations results would help the diagnosis of alcoholic hepatitis?

A

Raised bilirubin
Raised GGT and ALP
Alcohol history

397
Q

What is the treatment for alcoholic hepatitis?

A 
Supportive
Treat infection
Treat encephalopathy
Treat alcohol withdrawal
Protect against GI bleeding
Airway protection
398
Q

When do you give steroids for alcoholic hepatitis?

A

Only if grading severe e.g. Glasgow Alcoholic Hepatitis Score >9

399
Q

What scoring system is used to determine the prognosis of alcoholic hepatitis and whether to use steroids?

A

Modified Maddrey’s discriminant function

400
Q

Which nutrient are alcoholic hepatitis patients often lacking?

A

Thiamine

GI (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions