GI Flashcards

1
Q

Causes of small bowel obstruction

A

Adhesions

Hernias

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

Causes of large bowel obstruction

A

Colon ca
Constipation
Diverticular stricture
Volvulus

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

Features of small intestines on X-ray

A

Around 2.5cm (vertebrae height)
Central
Multiple loops
Valvuli coniventers (across the lumen)

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

Large intestine features on X-ray

A

Larger calibrate around 6cm
Peripheral
Semi- lunar folds (haustra)

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

Upper GI bleeding causes

A

Peptic ulcers
Mallory-Weiss tear
oesophageal varices
drugs (NSAIDs, aspirin, steroids, thrombolytics, anticoagulation)

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

Rockall risk score pre endoscopy

A

Age 0pt: <60yrs, 1pt: 60-79 2pts: 80+
Shock (systolic&pulse) 0pts: >100&<100 1pt: >100 both, 2pts: <100 systolic
Co-morbidity 0pts: nil, 1pt: heart failure, IHD, 2pts: renal/liver failure, 3pts: mets

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

Rockall score post-endoscopy

A

Diagnosis 0pts: Mallory-Weiss tear/ no lesion/ no recent bleed, 1pt: all other, 2pts: GI malignancy
Recent haemorrhage signs: 0pts: none/dark red spots, 2pts: blood/ adherent clot/ visible vessel

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

Varices: high risk of re-bleeds features

A
  • active arterial bleed
  • visible vessel
  • adherent clot/black clots
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Child- Pugh score, what is it for?

A

Progression of liver cirrhosis

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

Child- Pugh score

A
1pt.        2pts.        3pts. 
Bilirubin   <34.      34-51.        >51 
Albumin.  >35       28-35.       <28 
Prothrombin 
time inc (s) 1-3.      4-6.         >6 
Ascites.      --          Slight.    Moderate 
Encephalopathy 
(Grade)      --         1-2.           3-4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Haemorrhaging shock classification

A

Blood loss (%loss)

Class I <15%
Class II 15-30%
Class III 30-40%
Class IV >40%

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

Murphy’s sign

A

Acute cholecystitis
RUQ Compression on inspiration
Positive if painful

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

Boas’ sign

A

Acute cholecystitis
Pain in the tip of r. scapula
Hyperaesthesia

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

Grey-Turner’s sign

A

Acute pancreatitis
Bruising/discolouration
Flanks

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

Cullen’s sign

A

Acute pancreatitis
Bruising/discolouration
Around the umbilicus

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

Rosvig’s sign

A

Acute appendicitis

LIF palpating -> RIF pain

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

Signs of peritonitis

A
Rebound tenderness 
Rigidity 
Guarding 
Positive cough test 
Pain worse with any movement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Antibiotics for suspected peritonitis

A

Metronidazole + cefuroxime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Abdo trauma: investigation of choice

A

CT abdomen

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

Abdo trauma: focused abdominal sonography for trauma (FAST), where does it look?

A
4Ps 
Morison's pouch 
Pouch of Douglas 
Perisplenic
Pericardium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Trousseau’s sign of latent tetany

A

Sign of hypocalcaemia (e.g. In malignancy)
BP cuff inflated to above pt’s systolic BP
Held for 3 mins
Brachial artery occluded
Hypocalcaemia induces neuromuscular irratibility causing muscle spasm
Wrist and MCP flexes
PIP and DIP joints extend

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

GORD causes (4)

A
  1. lower sphincter dysfunction/ loss of peristalsis/ slow emptying
  2. hiatus hernia/ obesity/ overeating
  3. alcohol/ drugs (tricyclics, nitrates, anticholinergics)
  4. pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

GORD management

A

OTC: antacids, alginates, H2 antagonists
PPI
Metoclopramide (decreases muscle tone and helps with gastric emptying)
Surgery to increase resting muscle tone

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

Barrett’s oesophagus cell change

A

Stratified squamous cell to simple columnar metaplasia

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

Barrett’s oesophagus: what criteria is used

A

Barrett’s oesophagus: what criteria is used

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

Prague criteria: what is it for?

A

Barrett’s oesophagous

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

Prague criteria outline

A

Locate gastro-oesophageal junction
Circumfermental metaplasia distance
Maximal extend metaplasia distance

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

Barrett’s oesophagous management

A
PPI 
Metoclopramide
Annual surveillace (low grade changes)
Resection of high grade changes 
Others: ablation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Achalasia: define

A
  • oesophageal motility disorder
  • failure of the lower sphincter relaxation
  • leads to oesophageal dilatation and uncoordinated peristalsis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Achalasia: what does it involve?

A

degeneration of myenteric plexus

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

Achalasia treatment

A

balloon dilatation
surgical myotomy
botulin toxin injection

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

Diffuse oesophageal spasm features

A

intermittent motility disorder

symptoms with hot or cold food

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

Los Angeles classification: what is it for?

A

GORD

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

What classification is used for GORD?

A

Los Angeles classification

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

Los Angeles classification outline

A
  1. Max 1 mucosal break <5mm long not exceeding over <2 mucosal fold tops
  2. Mucosal break > 5mm, <2mucosal fold tops
  3. Mucosal break over 2 mucosal tops
  4. Break over >75% of the circumference
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Sliding hiatus hernia define

A

Hernia through the diaphragmatic hiatus with the gastro-oesophageal junction in the chest cavity

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

Rolling hiatus hernia

A

Stomach herniation anteriorly
Cardiac in normal position
Sphincter intact- no GORD symptoms
Can strangulate

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

Hiatus hernia management

A

Surgery if pts get obstructive symptoms or have reduced lung capacity
NG tube for emergency decompression

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

Oesophageal perforation cause

A

Iatrogenic (50%)

Spontaneous from vomiting

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

Oesophageal perforation consequences

A
Shock, cyanosis, sepsis
Pneumothorax
Pleural effusion
Medinastitis
Peritonitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Suspected oesophageal perforation investigations

A

erect CXR

CT +/- contrast swallow

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

Oesophageal perforation management

A
oesophagogastric centre transfer 
cervical: NBM + IV fluids + Abx
Thoracic: as above + stent or surgical repair 
- drainage
- anti-fungals
- jejunostomy feeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Peptic ulcer: define

A

ulcers to columnar mucosa in the lower oeasophagus, stomach, duodenum or small bowel.
Usually die to action of acid
Include gastric and duodeneal ulcers

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

Duodenal ulcer: the usual location

A

1st part of duodenum

50% on the anterior wall

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

Duodenal ulcer: endangered artery

A

gastroduodenal artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Gastric ulcer: usual location

A

lesser curvature (distal half)

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

Gastric ulcer: endangered arteries

A

splenic

Right and left gastric

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

Duodenal ulcer: malignant potential?

A

Rarely

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

Gastric ulcer: malignant potential?

A

Yes

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

Duodenal ulcers: course

A

Acute or chrnoic

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

Gastric ulcer: course

A

Always chronic

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

Peptic ulcer: causes

A
H. pylori 
NSAIDs
Smoking
Hyperparathyrodism 
Blood group O
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How does H.pylori cause ulcers?

A

H.pylori sits in gastric mucosa

  • > gastritis
  • > G cell stimulaition
  • > increased acid secretion
  • > gastric metaplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

How do NSAIDs cause ulcers?

A

NSAIDs inhibit prostaglandin secretion
by inhibiting cyclo-oxygenase
Prostaglandins are involved in mucus and bicarbonate production
-> protective mechanisms are reduced

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

How does hyperparathyrodism cause ulcers?

A

increased Calcium levels

-> acid secretion stimulated

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

Clinical features of gastric ulcers

A

pain when eating

reduced by vomiting

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

Clinical features of duodenal ulcers

A

pain when hungry

reduced by food, antacids, milk and vomiting

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

Suspecteed peptic ulcer investigations

A

Endoscopy + biopsy (to exclude malignancy)
H.pylori testing
- CLO test

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

Explain H.pylori testing

A

Biopsy sample placed urea
Ammonia released by H.pylori
-> colour change

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

Peptic ulcer medical management

A

Diet (alcohol, smoking, avoid NSAIDs)
PPI- omeprazole 20mg
H2 blockers- renitidine
H.pylori eradication if positive

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

H. pylori eradication

A

PPI
Metronidazole
Clarithromycin

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

Peptic ulcer surgical management

A

endoscopic dilatation

pyloroplasty +/- vagotomy

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

Zollinger-Ellison syndrome cause

A

gastin-secreating tumour (gastroma)

- usually intra-pancreatic or stomach/duodenum

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

Zollinger- Ellison syndrome has association to what other syndrome ?

A

MEN syndrome (multiple endocrine neoplasia)

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

Zollinger-Ellison syndrome symptoms

A

Diarrhoea- caused by increased levels of acid in intestine
Steatorrhoea- inactivation of lipase by acid
Ulcer symptoms

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

Zollinger-Ellison diagnosis and investigation

A

problematic diagnosis

  • unusal ulcer sites at young age
  • persistent ulcers

Serum gastrin levels
CT/MRI to localise tumour

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

Zollinger- Ellison syndrome manaement

A

Tumour excision

PPI

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

Peptic ulcer: perforation normally associated with which ulcer?

A

Duodenal

Perforations are rare with peptic ulcers

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

Ulcer perforation: clinical features

A
Epigastric and shoulder tip pain
Peritonitis (pale, shocked, peripheral shut down) 
Appendicitis features (stomach contents in the r. paracolic gutter)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Ulcer perforation investigations and diagnosis

A

Erect CXR -> pneumoperitoneum
Amylase -> moderate hyperamylasaemia
Contrast meal/CT if diagnosis uncertain

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

Ulcer perforation initial management

A

Peritonitis: ABCDE, oxygen, IV fluids, Abx, NG tube
Opiate analgesia
IV PPI

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

Duodenal ulcer perforation: surgical management

A

sutured close with omental patch

consider gastrotomy

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

Gastric ulcer perforation: surgical management

A

sutured close with omental patch (prepyloric)
local excision (body)
15% will be malignant
-> gastric resection if biopsy positive

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

Gallstones: pathophysiology

A

result of imbalance of the constituents of bile

e.g. inability to keep cholesterol in the micellar form in GB

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

Gallstones complications in the GB and cystic duct (6)

A
Biliary colic 
Cholecystitis 
Mucocoele 
Empyema 
Carcinoma
Mizzi's syndrome (GS impacted in the cystic duct -> compression of th CBD -> obstructive jaundice)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Mizzi’s syndrome

A

GS impacted in the cystic duct

  • > compression of th CBD
  • > obstructive jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Gallstones complications in the bile duct (3)

A

obstructive jaundice
cholangitis
pancreatitis

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

Gallstones complications in the gut (1)

A

Gallstone ileus

  • > GS errodes through the GB into duodenum
  • > terminal ileum obstruction
  • > duodenal obstruction (Bouveret’s syndrome)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Bouveret’s syndrome

A

Duodenal obstruction caused by GS eroding though thr GB and into duodenum

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

Acute cystitis definition

A

inflammation of the gallbladder caused by a stone impaction in the neck of GB

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

Acute cystitis features

A

pain (r. hypochondrial) and fever
Murphy’s sign
phlegmon (RUQ mass of inflammed omentum)

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

Acute cystitis natural progression

A

Resolves within 4-5d normally

can progress to gangrene/ empyema

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

Acute cystitis management

A

cholecystectomy

percutaneous drainage if unfit for surgery

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

Biliary colic definition

A

Intermittent pain caused by transient obstruction of GB from an impacted stone
without inflammation

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

Biliary colic complication

A

Acute cholecystitis

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

Bile production

A

Bile-acid dependent component (bile acids and pigments)

  • hepatocytes
  • kupffer cells (Hb breakdown to heme and globin. Heme broken into bilirubin, conjugated to glucoronic acid and secreted into bile)

Bile acid independent component
- alkaine juice from duct cells

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

What do micelles contain

A

anaphilatic bile salts

Anaphobic: cholesterol, phospholipids, bile pigments

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

Flow of bile

A
bile secreted into canicli 
reach terminal duct
leave the liver via the transverse fissure 
left and right hepatic ducts merge 
common hepatic duct 
->GB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Obstructive jaundice cause

A

stone blocking CBD

cholangiocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Courvoisier’s law

A

palpable GB + jaundice

  • > cause is unlikely to be a stone
  • > suggestive of malignancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Ascending cholangitis definition

A

Bile duct infection
Caused by obstructed bile flow
-> increased pressure
allows for bacterial contamination and bacteraemia

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

Ascending cholangitis features

A

Charcot’s triad

RUQ pain, fever and jaundice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Charcot’s triad: what does it suggest and what features are present?

A

Ascending cholangitis

RUQ pain, fever and jaundice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Acute pancreatitis causes

A
Gallstones 
Ethanol
Trauma
Steroids
Mumps
Autoimmune 
Sphincter Oddi dysfunction/scorpion bites
Hypercalcaemia/lipidaemia
ERCP
Drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Drugs which can cause acute pancreatitis

A
Azathioprine/mercaptopurine 
Corticosteroids 
Erythromycin/ trimethoprim / tetracycline 
Frusemide
Isonizid 
Metformin 
Opoids 
Sitagliptin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Acute pancreatitis: clinical features

A
epigastric pain -> back 
relieved by sitting forward
guarding &amp; tenderness 
Grey-turner's sign (l. flank ecchynosis)
Cullen's sign (periumbilical ecchynosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Grey-turner’s sign

A

Acute pancreatitis sign

L. flant ecchynosis

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

Cullen’s sing

A

Acute pancreatitis sign

Periumbilical ecchynosis

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

Acute pancreatitis investigations

A

Amylase (>1000 U or 3x upper limit of normal)- not always raised
Lipase
Alk. phos- raised suggests gallstone
CT (contrast- enhanced) -> oedema (necrosis)
AXB: absent psoas sign, colon cut-off sign, gallsotne or pancreatic calcification
USS (within 48h)- to identify a stone

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

Acute pancreatitis management

A
Morphine 
Fluids (large amounts)
NBM 
Nutritional support (enternal not TPN)
ERCP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Acute pancreatitis complications

A
Pancreatic necrosis 
pseudocyst 
abscess 
progressive jaundice 
GI bleeding 
GI ischaemia/fistula
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Chronic pancreatitis definition

A

chronic inflammatory condition of the pancreas characterized by fibrosis and exocrine pancreatic dysfunction

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

Chronic pancreatitis causes

A

Alcohol
smoking
rarely hereditary

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

Chronic pancreatitis pathophysiology

A

viscid pancreatic juice causes protein plugs in ducts

  • > calcification -> stones
  • > impaired pancreatic juice flow
  • > inflammation and stricture formation
  • > replacement of normal tissue by fibrous tissue
    • > loss of acinar tissue -> steatorrhoea
    • > loss of islet tissue -> DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Chronic pancreatitis clinical features

A
epigastric pain ->  back (relieved by leaning forward)
avoidance of fatty foods 
heat brings pain relief 
steatorrhoea 
DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Chronic pancreatitis diagnosis and investigations

A

CT: speckled calcification +/- inflammatory changes +/- pseudocyst
MRCP: pancreatic duct stricture
Random blood glucose for monitoring
Fecal fat excretion measurement

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

Chronic pancreatitis management

A
abstinence from alcohol
non-opiate analgesia 
creon (pancreatic exocrine supplement) 
endoscopic: stent 
surgery to relieve pain and compression 
- drainage and roux limb of jejunum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Appendix location

A

posterio-medial wall of cecum
2cm below ileocaecal valve
at McBurney’s point (1/3 along a line drawn between the right anterior superior iliac spine and the umbilicus)

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

McBurney’s point location

A

1/3 along a line drawn between the right anterior superior iliac spine and the umbilicus

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

What’s inside the appendix?

A

Lymphoid follicles in the submucosa
abundant in children
atrophy with age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Appendicitis: clinical features

A

Generalised pain -> localises to McBurney’s point
Rovsing’s sign
Psoas stretch sign

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

What causes pain in acute appendicitis to localise to McBurney’s point?

A

Inflammation of the parietal peritoneum

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

Rovsing’s sign

A

Acute Appendicitis

LIF palpation causes pain in the RIF

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

Psoas stretch sign

A

Acute Appendicitis

painful hip flexion

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

Acute appendicitis managemen

A

appendicectomy
IV fluids
Abx (metronidazole)

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

Meckel’s diverticulum

A
2% of the population
2 inches (5cm) long
2 feet (60cm) from ileocecal valve 
2/3 have ectopic tissue 
- 2 types of ectopic tissue: gastric or pancreatic 
2% become symptomatic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Colovesicular fistula: define

A

fistula between the colon and the bladder

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

Colovesicular fistula: common cause

A

diverticular disease complication

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

Colovesicular fistula: symptoms

A

dysuria
cloudy urine
bubbling on mictuition

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

Colovesicular fistula: diagnosis

A

barium enema

cystoscopy

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

Colovesicular fistula: management

A

resection of the affected colon region and bladder repair

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

Bowel ischaemia: cause

A

atheroma at the origin of the inferior mesenteric artery

leads to gangrene and perforation

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

Bowel ischaemia: clinical features

A

General: abdo pain, nausea, vomitting

red currant jelly bloody diarrhoea

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

Angiodysplasia in the colon: define

A

anteriovenous malformations

lead to bleeding

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

Angiodysplasia: diagnosis

A

Colonoscopy by visualising a bleeding point

Angiography

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

Angiodysplasia: management

A

angiographic embolisation
injection sclerotherapy
emergency laparotomy

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

Diverculosis: define

A

presence of divericula in the colon

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

Diverticular disease: define

A

symptomatic diverticula

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

Diverculitis: define

A

inflammation of a diverticulum

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

Diverticular disease: common location and reason

A

sigmoid
high intramural pressure
rectum normally spared

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

Diverticular disease: reason for rectal sparing

A

different arrangement of blood vessels

outer longitudinal smooth muscle encompasses the full circumference of the rectum

132
Q

Diverticular disease: clinical features

A
general: abdo pain, nausea 
fever, loose stools -> acute diverticulisis 
bleeding pr (dark red clotted blood)
133
Q

Diverticular disease complications

A
  • diverticulitis
  • pericolic/paracolic abscess
  • perforation/peritonitis
  • fistula
  • strictures
134
Q

Diverticular disease management

A

diet high in fibre
antispasmodics
laxatives
resection if persistent symptoms

135
Q

Volvulus common location

A

sigmoid (around sigmoid mesentery)

136
Q

Caecum volvulus

A

around the SMA in anticlockwise direction

rare

137
Q

Volvulus management

A

decompression with sigmoidoscopy

138
Q

Familial Adematous Polyposis (FAP) mutation and consequences

A

APC gene mutation (chromosome 5)
Wnt signalling pathway
-> 90% chance of developing adenocarcinoma by the 3rd-4th decade

139
Q

FAP management

A

surgical prophylaxis- colon excision

140
Q

FAP extra-colonic features

A
  • gastric fundus polyps

- antral and duodenal adenomas

141
Q

Adenomatous polyps, what conditions are they found in?

A

usually sporadic
FAP
HNPCC (hereditary non polyposis colorectal cancer) AKA Lynch syndrome

142
Q

Adenomatous polyps: features

A

caused by XS growth of colorectal epithelium

precursor for colonic cancer

143
Q

Juvenile polyposis syndrome: type of polyps and description

A

hamartomatous polyps

excesive amounts of the normal architectural components

144
Q

Juvenile polyposis syndrome: inheritance pattern

A

autosomal dominant

145
Q

Juvenile polyposis syndrome: consequences

A

50% lifetime risk of colorectal ca

146
Q

Juvenile polyposis syndrome: management

A

surveillance

prophylactic surgery

147
Q

Peutz-Jaghers syndrome: mutation and inheritence pattern

A
autosomal dominant 
LKB1 gene (chromosome 19)
148
Q

Peutz-Jaghers syndrome: manifestations

A

GI polyps
- commonly in jejunum
- hamartomas (XS growth of normal architectual components)
Melanin pigmentation at mucocutaneous junctions (eyes and mouth)

149
Q

Peutz-Jaghers syndrome: consequences

A

increased risk of cancer of:

  • colorectal
  • gastric
  • pancreatic
  • breast
  • ovarian
150
Q

Peutz-Jaghers syndrome: symptoms

A
dark brown/blue spots on the lips/ inside of the mouth 
abdo pain
obstruction (interssusception) 
rectal bleeding 
iron deficiency anaemia
151
Q

Important to consider what, in AF patients with abdo pain?

A

mesenteric ischaemia

152
Q

Mesenteric ischaemia: vessel commonly affected?

A

superior mesenteric artery -> small bowel

153
Q

Mesenteric ischaemia: causes

A

thrombotic
embolic
non-occlusive in low flow states
other: trauma, strangulation (volvulus or hernia)

154
Q

Mesenteric ischaemia: classical triad

A

acute severe abdo pain
no abdo signs
rapid hypovolaemia -> shock

155
Q

Mesenteric ischaemia: tests

A

increased Hb (due to plasma loss)
increased WCC
modestly increased amylase

156
Q

Haemorrhoids define

A

excessive amounts of the normal endoanal cushions

comprise anorectal mucosa, submucosal tissue and submucosal blood vessels

157
Q

Haemorrhoids pathophysiology

A

degeneration of fibro-elastic tissue and smooth muscle

158
Q

Haemorrhoids: predisposing features

A

constipation
chronic straining
obesity
pregnancy (increased connective tissue laxity)

159
Q

Internal haemorrhoids definition

A

confined to the tissue of the upper anal canal

160
Q

Haemorrhoids clinical features

A
  • bleeding pr- bright red on wiping
  • prolapse
  • irritation features (pruritis, mucus, discharge, perianal discomfort)
161
Q

Haemorrhoids investigations

A

DRE to exclude other conditions
Rigid sigmoidoscopy/proctoscopy -> diagnosis
Flexible sigmoidoscopy/colonoscopy (atypical features, >55y.o ?cause)

162
Q

Haemorrhoids: management based on degree

A

1st/ thrombosed piles: medical: consitipation aoidance, bulking laxitives, high fibre diet or
2nd: banding, dilute penthol injections
3rd/4th: haemorrhoidectomy

163
Q

Haemorrhoids stages (degrees)

A

1st: bleeding, visible on proctoscopy but don’t prolapse
2nd: prolapse, spontaneous reduction
3rd: prolapse: manual reduction
4th: irreducibly prolapsed

164
Q

Anorectal internal sphincter: muscle type , innervation and relaxants

A
smooth muscle (involuntary)
circular 
pelvic autonomic supply 
relaxants: nitic oxide donours (GTN) and calcium antagonists (diltazem)
165
Q

Anorectal external sphincter: muscle type, innervation and relaxants

A
skeletal muscle (volountary)
-> blends with puborectalis 
- surrounds the lower 2/3 anal canal
pudendal nerve supply (S2, 3, 4) 
relaxants: botulin toxin
166
Q

Anorectal canal: arterial supply

A

above pectinate line: superior rectal a. (IMA branch)
below pectinate line: inferior rectal a. (internal pudental branch)
both anastimose with middle rectal a.

167
Q

Anorectal canal: venous drainage

A

above pectinate line: superior rectal v. -> inferior mesenteric v.
below pectinate line: inferior rectal v. -> inferior pudental v.

168
Q

Anorectal canal: nerve supply

A

above pectinate line: inferior hypogastric plexus (visceral inn.)
below pectinate line: anferior anal n (pudental nerve branch- somatic)

169
Q

Anorectal canal: lymphatics

A

above pectinate line: internal iliac l.n.

below pectinate line: superficial inguinal l.n.

170
Q

Fistula-in-ano: define

A

an abnormal connection between two epithelial surfaces

to perianal or vaginal skin

171
Q

Fistula-in-ano: pathophysiology

A

sepsis in an anal gland abscess pushes through

172
Q

Fistula-in-ano: clinical features

A

perianal ‘pressure’ sensation

chronic perianal discharge (seropurulent via punctum)

173
Q

Fistula-in-ano: investigations

A

perineum and rectum investigation under anaesthesia
endoanal USS
MRI (most sensitive)

174
Q

Fistula-in-ano: management

A

abx (symptomatic)
abscess drainage
seton suture -> allows drainage
fistulotomy to remove granulation tissue

175
Q

Fissure-in-ano: define, location within canal and features

A
lineal anal ulcer 
in the canal below the dentate line 
usually the posterior wall 
(anterior after childbirth)
little granulation tissue 
-> fistula
176
Q

Fissure-in-ano: clinical features

A

skin tags (sentinel pile) frequently present
outlet pr bleeding
DRE too painful when active
defecation avoidance -> overflow incontinence (children)

177
Q

Fissure-in-ano: management

A

acute: self resolving
only treat chronic (>6wks)
stool softeners
diltiazem/nitrates for sphincter relaxation
botulin toxin
sphincterectomy (int. sphincter division)
-> anal incontinece risk
anal advancement flap or rotational flap to cover the fissue with well vascularised skin

178
Q

Crohn’s disease: pathological features

A
cobble stone appearance 
- skip lesions 
- oedematous islands 
deep fissure ulcers 
transmural inflammation 
granulomas
mucosal thinckening -> fibrosis
179
Q

Crohn’s disease: definition

A

Inflammatory bowel disease

chrnoic inflammatory non-caseating granulomatous disease affecting any part of the GI tract

180
Q

Crohn’s disease: peak incidence

A

teens

early 20s

181
Q

Crohn’s disease: risk factors

A

smoking

family history

182
Q

Crohn’s disease: clinical features

A
chronic disease with exacerbations
diarrhoea +/- mucus or blood 
abdo pain
tenderness
tenesmus 
malabsorption (vit B12)

children: failure to thrive

183
Q

Crohn’s disease: extra-interstitial manifestations

A

erythema nedosum
primary biliary cirrhosis
polyarthritis/ ankylosing spondylitis
chronic active hepatitis

184
Q

Crohn’s disease: investigations

A
anaemia 
increased acute-phase proteins (inc. CRP, WCC)
barrium follow through 
MRI w oral osmotcally active agents 
sigmoidoscopy/colonoscopy 
video capsule endoscopy 
CT colonography
185
Q

Crohn’s disease: findings on barrium follow through

A

rose thown ulcers
terminal ileal strictures
mucosal thickening/ luminal narrowing

186
Q

Crohn’s disease: medical management

A

glucocorticosteroids or 5-ASA (induce remission)
azathioprine or mercaptopurine (adjunct to induce remission/ maintenance)

consider methotrexate/ infliximab

187
Q

Crohn’s disease: surgical management indications (4)

A
Acute/ emergency: 
-> fulminant colitis, haemorrhage, obstruction 
Subacute:
-> symptomatic reflief if medication fails 
Chronic 
-> ca prophylaxis, steroid dependency 
Perianal disease 
->abscess, fistula, anorectal stricture
188
Q

UC: pathological features

A
columnar mucosal and submucosal inflammation 
crypt abscess 
-> architectural distortion
-> ulceration 
goblet cell depletion
189
Q

UC: definition

A

inflammatory bowel disease
chronic inflammatory condition affecting the columnal mucosa and submucosa of the rectum and extends proximally in continuity
occasional rectal sparing

190
Q

UC: peak incidence

A

any age

peaks in early adulthood and 60s

191
Q

UC: association to smoking

A

smoking is protective

first presentation around 6m after quitting is common

192
Q

UC: clinical features

A

chronic condition with exacerbations
diarrhoea with blood and mucus
intermittent pyrexia
incapacitating fecal urgency and frequency

193
Q

UC: rectal complications

A

thick mucosa
contact bleeding
loss of rectal mucosal vessels (sigmondoscopy)

194
Q

UC: investigations

A
sigmoidoscopy/colonoscopy + biopsy for diagnosis 
-> loss of haustra
anaemia 
acute protein proteins (WCC, CRP)
AXR -> thumb-printing, rigler's sign
Barium enema -> lead pipe appearance
195
Q

Thumbprinting on AXR suggests what?

A

mucosal thickening

eg UC

196
Q

Lead pipe appearance (barium enema) suggests what?

A

loss of haustra in UC

197
Q

UC proctitis/colitis management

A

topical steroids/ 5- ASA
suppositories or enema

prednisolone PO if required

198
Q

Pancolitis (severe UC) management

A

topical steroids/ 5- ASA (suppositories or enema)
systemic steroids/5-ASA
azathioprine/ mercaptropurine
cyclosporin (red. lymphocyte function) or infliximab

199
Q

Acute severe colitis management

A

IV hydrocortisone 100mg QDS
IV cyclosporin
IC/PO metronidazole (if infective)

200
Q

What is Rigler’s sign (AXR) and what does it suggest?

A

perforation

air on inside and outside of the wall

201
Q

UC: surgery indications

A
  • acute/chronic- not responsive to medical therapy
  • recurrent exacerbations
  • high-grade dysplasia or ca
202
Q

Trousseau sign of malignancy

A

Thrombophelbitis migrans

cancers associated with hypercoagulopathy (unknown mechanism)

203
Q

Haematoma of rectus sheath: pathophysiology

A

spontaneous or traumatic
rupture of an inferior epigastric artery branch

(eldery on anticoags.)

204
Q

Desmond tumour definition

A

arises from fibrous intramuscular septa in the lower rectus abdomnis

malignant potential (fibro sarcoma)

205
Q

Desmont tumour management

A

wide excision

206
Q

Hernia: define

A

abnormal protrusion of a viscous or its part though a weaknes in its containing wall

207
Q

Reducible hernia: define

A

contents can be restored

208
Q

Incarcerated hernia: define

A

part or all of the contents can’t be reduced

due to a narrow neck or adhesions

209
Q

Strangulated hernia: define

A

blood supply affected

usually caused by a tight neck of the peritoneal sac

210
Q

Hernia perforation sequence

A

venous and lymphatic occlusion

  • > oedema and increased venous pressure
  • > impeding arterial flow
  • > bowel necrosis and perforation
211
Q

Inguinal hernia presentation

A

lump above inguinal ligmament

+/- ache

212
Q

Inguinal hernia investigations

A

USS

+/- CT, MRI

213
Q
Inguinal canal boarders:
anterior 
posterior
roof 
floor
A

anterior: aponeurosis of the external oblique
posterior: transversialis fascia (deep ring)
roof: tranverscialis fascia, transverscialis abdominis and internal oblique
floor: inguinal ligament and lacunar ligament (medially)

214
Q

Hasselbach’s triangle boarders

A

medial to inferior epigastric a
rectus sheath
inguinal ligament

215
Q

What runs through the superficial ring?

A

Spermatic duct or round ligmant

216
Q

Which hernias occur through the Hasselbach’s triangle?

A

Direct inguinal hernia

217
Q

Aetiology of indirect inguinal hernia

A

Congenital

Patent processus vaginalis

218
Q

Which of the inguinal hernias is more likely to strangulate and why?

A

Indirect hernia

Narrow neck

219
Q

Inguinal hernia management

A

Open/laparoscopic mesh repair

herniotomy (infants)

220
Q

What makes up rectus sheath?

A

appeneuroses of:

  • external oblique
  • internal oblique
  • transversus abdominis
221
Q

Arcuate line

A

arch of fibres in the abdominal wall
half way between the umbilicus and pubic symphysis

place where rectus sheath no longer contains rectus abdominis (above) and now lies superficial to it (below)

222
Q

Pyramidalis: location

A
2nd vertical muscle in the abdominal wall
triangular muscle 
anterior to rectus abdominis 
at the base of the pubis 
attached to linea alba
223
Q

Abdominal wall nerve supply above the umbilicus

A

T7-9

224
Q

Abdominal wall nerve supply around the umbilicus

A

T10

225
Q

Abdominal wall nerve supply below the umbilicus

A

T11-12 & L1

226
Q

Scrotum/ Labia majora nerve supply

A

L1 (illio-inguinal nerve)

227
Q

Femoral hernia location

A

below inguinal ligmaent
lump inferior and lateral to pubic tubercle
via femoral canal (which is in the femoral triangle)

228
Q
Femoral canal: location, contents and boarders
medial 
lateral
anterior
posterior
A
Located within the femoral triangle 
Contains deep inguinal lymph node 
medial- lacunar lig
lateral- femoral v
anterior- inguinal lig
posterior- pectineal lig and pectineus muscle
229
Q
Femoral triangle: contents and boarders
superior
lateral 
medial 
roof 
base
A

Contains NAVEL (femoral nerve, artery, vein, empty space, lymph canal)
superior- inguinal lig
lateral- sartorius
medial: adductor longus (med. boarder)
roof: fascia lata
base: pectineus, illiopsoas and adductor longus

230
Q

Femoral hernia management

A

all require repairing
-> hernia reduction and narrowing of the femoral cnal
approach above the inguinal lig (McEcedy approach)

Interrupted sutures
suture plication
mesh plug

231
Q

True umbilical hernias: define and natural progression

A

congenital in infants
95% close by age of 3
if not excise sac and close the defect in the abdo fascia

232
Q

Paraumbilical hernia: aetiology and natural progression

A

acquired weakness
obese multiparous women
enlarge in size -> thinning the skin as they do

233
Q

Paraumbilical hernia: management

A

risk of strangulation

-> laparoscopic mesh repair

234
Q

Epigastric hernia: definition

A

defects in the linea alba between the xiphisternum and the umbilicus

235
Q

Epigastric hernia: risk of hstrangulation and management

A

moderate risk of strangulation

laparoscopic intraperitoneal mesh or non0absorbable sutures

236
Q

Oesophageal carcinoma types and locations

A

squamous cell- upper 2/3

adenocarcinoma- lower 1/2

237
Q

Risk factors for oesophageal SCC

A

smoking
alcohol
diet (preserved food with nitrates and low in oxidants)

238
Q

Risk factors for oesophageal adenocarcinoma

A

GORD
Barrett’s
obesity
achalasia

239
Q

clinical features of oesophageal carcinoma

A

progressive dysphagia
hoarseness (recurrent laryngeal nerve)
neck swelling (SVC obstruction)
Horner’s syndrome (sympathetic chain)

240
Q

Investigations for suspected oesophageal cancer

A

endoscopy + biopsy
USS for local invasion
CT/PET for mets
laparoscopy for peritoneal mets

cytology of enlarged lymph nodes (if positive surgical excision contraindicated)
barrium swallow if failed intubation or suspected post-cricoid ca

241
Q

Indications for barrium swallow in oesophageal cancer

A

failed intubation

suspected post-cricoid cancer

242
Q

Oesophageal cancer: resection contraindications

A

positive cytology of lymph nodes

243
Q

Potentially curative management of oesophageal cancer

A

neoadjuvant chemo

resection or ablation

244
Q

Palliative management of oesophageal cancer

A
for dysphagia:
-endoluminal self exdanding stenting 
-external beam radiotheraphy 
symptomatic mets:
-chemo
245
Q

Oesophageal cancer prognosis

A

poor
<10% 5 year survival
due to late presentation

246
Q

Dysphagia: red flags

A

progressive
weight loss
painful
neurological (acute to both fluids and solids or associated neurological symptoms)

247
Q

Gastric adeocarcinoma risk factors

A

h. pylori
diet: pickled or salt preserved food
chronic gastritis

248
Q

Gastric adenocarcinoma clinical features

A

dyspepsia (new onset in over 55yo)
trosier’s sign/ enlarged Virchow’s node
sister Joseph’s nodule (periumbilical mass)

249
Q

Gastric adenocarcinoma investigations

A

endoscopy + multiple (>6) biopsies of ulcer edge
CT for mets
EUS for invasion depth
Laparoscopy for peritoneal mets assessment

250
Q

Gastric adenocarcinoma TNM (P/H) staging

A

T: 0- mucosa, 1- submucosa, 2- muscle, 3- serosal surface, 4- other organs
N: 0- no l.n., 1- <3cm from primary, 2- >3 cm
P: peritoneal mets
H: hepatic pets

251
Q

Gastric adenocarcinoma management

A

neoadjuvant chemo
radical gastrectomy
post-op chemo
palliative chemo for disseminated diease in advanced ca

252
Q

Gastric adenocarcinoma early disease definition and prognosis

A

no mets

>90% 5-year survival

253
Q

Gastric adenocarcinoma advanced disease definition and prognosis

A

T3 +, N2 +, P1+, H1+

<25% 5-year survival

254
Q

Gastric ca: Gastrointerstitial stromal tumours (GIST) aetiology

A

arise from pacemaker cells
usually submucosal
variable natural history

255
Q

What type of gastric ca arises from pacemaker cells?

A

Gastrointerstitial stomal tumours (GIST)

256
Q

Gastrointerstitial stromal tumours (GIST): management

A

small (2-5cm)- survaillence

big (>5cm) or symptomatic - resect

257
Q

Gastric ca: carcinoid tumour aetiology

A

nauroendocrine orginin

malignant potential

258
Q

What is carcinoid syndrome caused by?

A

serotonin overproduction

259
Q

Gastric lymphoma: aetiology

A

many arise from MALT
commonest site of GI lymphomas
H.pylori association (eradication can cure it)

260
Q

Gastric lymphoma: management

A

H.pylori eradication

High grade -> chemo

261
Q

Hepatocellular carcinoma risk factors

A

cirrhosis (2/3)
chronic viral hepatitis
alcohol
alfatoxin, contraceptives & androgens

262
Q

Hepatocellular carcinoma origin

A

liver parenchymal cells

263
Q

Hepatocellular carcinoma presentation

A

rapid deterioration of pre-exisiting cirrhosis

264
Q

Hepatocellular carcinoma investigations

A
LFTs 
alpha-fetoprotein (early detection in susceptible individuals)
USS
CT/MRI
needle aspiration (if not for resection)
265
Q

Hepatocellular carcinoma management

A

curative (if no mets and technically possible)
- partial hepatectomy
- transplant
Palliative: embolisation

266
Q

Hepatocellular carcinoma prognosis

A

45% 5-year survival if resectable

267
Q

Cholangiocarcinoma origin

A

intra- or extra- hepatic billiary tree ducts

268
Q

Cholangiocarcinoma risk factors

A

chronic parasitic infection

cysts

269
Q

Cholangiocarcinoma typical sites

A

distal CBD
common heptic duct
confluence of hepatic ducts (Klatskin tumour)

270
Q

Cholangiocarcinoma clinical features

A
painless progressive jaundice 
advanced:
-pruritis
-pain/cholangitis
-weight loss
-ascities
271
Q

Cholangiocarcinoma investigations

A

USS

CT/MRI

272
Q

USS findings suggestive of Cholagiocarcinoma

A

intrahepatic duct dilatation

collapsed gallbladder

273
Q

Cholangiocarcinoma management

A

whipple operation
hepatic resection+roux limb of jejunum
palliation: stents

274
Q

Metastatic liver disease: origin

A
colorectal
pancreas 
stomach 
breast
oesophagus
275
Q

Metastatic liver disease: chances of mets elsewhere

A

90%

276
Q

Metastatic liver disease: clinical features

A
hepatomegaly + tenderness 
ascites
jaundice 
cachexia
pyrexia (10%) 
alk phos increased
277
Q

Metastatic liver disease: investigations

A
alk phos increased
needle biopsy/ aspiration cytology
-> diagnostic confirmation 
USS/CT 
-> extend of disease
278
Q

Metastatic liver disease: management

A
limited for advanced disease 
liver resection 
- must exclude extrahepatic involvement (CT chest/abdo/pelvis + colonoscopy)
chemotherapy 
pre op portal embolisation
279
Q

Pancreatic cancer types

A

ductal adenocarcinoma

pancreatic neuroendocrine tumours (PET)

280
Q

Pancreatic ductal adenocarcinoma: risk factors

A
smoking
age
high fat diet 
DM 
alcohol 
chronic pancreatitis
family history
281
Q

Pancreatic ductal adenocarcinoma: clinical features

A
obstructive jaundice (CBD obstruction) 
pain (epigastric, LUQ -> back, vague)
hepatomegaly (mets)
acute pancreatitis 
thrombophlebitis migrans (10%)
282
Q

Thrombophlebitis migrans

A

vessel inflammation due to blood clot (thrombophlebitis)
recurrent or appearing in different locations over time
sign of malignancy
Trousseau sign of malignancy

283
Q

Pancreatic ductal adenocarcinoma: investigations

A

serum CA19-9 (level correlates with ca volume)
abdo USS
doppler USS of portal vein and superior mesenteric vein
CT +/- FNB
ERCP +/- cytology

284
Q

Pancreatic ductal adenocarcinoma: management

A

currative (5%)
- whipple’s operation
- total/distal pancreatectomy
- adjuvant chemo
palliative
- jaundice (ERCP, stenting, percutaneous billiary drainage)
-duodenal obstruction (surgical gastric bypass)
-pain (oromorph, chemical ablation of the coeliac ganglioma)

285
Q

Pancreatic ductal adenocarcinoma: palliative pain management

A

oromorph

chemical ablation of the coeliac ganglioma

286
Q

Pancreatic neuroendocrine tumours (PET): facts

A

rare

usually malignant

287
Q

Pancreatic neuroendocrine tumours (PET): cause

A

sporadic or autosomal dominant
MEN type 1 (multiple endocrine neoplasia)
von Hippel Lindau
neurofibromatosis type 1

288
Q

Pancreatic neuroendocrine tumours (PET): clinical features

A

non-functional tumours: late diagnosis

functional tumours: depending on the hormone produced

289
Q

Small bowel tumours: types

A

adenocarcinoma
GIST (gastrointerstitial stromal tumours)
Lymphomas
Carcinoid tumours

rarely malignant

290
Q

Small bowel adenocarcinoma: origin

A

mucosa

pre-ampillary duodenum

291
Q

Small bowel adenocarcinoma: associations

A

FAP
Peutz-Jegher’s syndrome
Crohn’s
untreated Coeliac disease

292
Q

Small bowel adenocarcinoma: clinical features

A

present late often with mets
obstruction
recurrent abdo pain
GI bleeding

293
Q

Small bowel adenocarcinoma: management

A

surgical resection

palliative bypass

294
Q

Small bowel cancer: what is GIST?

A

Gastro-interstitial stromal tumours
arise from the connective tissue of GI wall
-> mesenchymal tissue, mesentery (smooth muscle, fibroblasts, lipocytes)

295
Q

GIST: tumour location

A
smooth muscle of gut 
50% gut
20-30% small bowel
10% rectum 
5% oesophagus
296
Q

GIST: maligancy association

A

c-kit mutation

tyrosine kinase inhibitos

297
Q

Small bowel lymphoma: usual type

A

non Hodgkins B-lymphomas

298
Q

Small bowel lymphoma: origin

A

MALT

mucose associated lymphoid tissue

299
Q

Small bowel lymphoma: associations

A

immune dysfunction conditions

300
Q

Small bowel lymphoma: clinical features

A

colicky pain
obstruction signs
GI bleed
systemic symptoms

301
Q

Small bowel lymphoma: management

A
depends on subtype and stage 
H.pylori eradication (can be helpful)
resection 
bone marrow transplant 
chemo
302
Q

Carcinoid tumours: origin

A

neuroendocrine tissue

submucosal enterochromaffin cells

303
Q

Carcinoid tumour: common locations (3)

A

appendix
Meckel’s diverticulum
duodenum (rare)

304
Q

Carcinoid tumour: associations

A

MEN type 1 syndrome

305
Q

What is carcinoid syndrome?

A

present in 10% carcinoid tumours
paraneoplastic syndrome
symptoms and signs due to carcinoid tumours
- flushing, diarrhoea, bronchal constriction, restrictive cardiomyophathy and right sided valvular heart disease (-> HF)
Caused by serotonin and kallikrein secretion

306
Q

Carcinoid syndrome diagnosis

A

24 hour urine lovels of 5-HIAA

307
Q

Carcinoid tumour: clinical features

A

vague symptoms of pain and weight loss

accidental finding

308
Q

Carcinoid tumour: management (inc. carcinoid crisis and syndrome)

A
resect w/ wide margin excision if possible 
IV octeotide - for crisis
somatostatin analogues- for synd. 
inteferon alpha
chemo
biological agents
309
Q

Small bowel tumours: investigations

A

CT chest/abdo -> primary identification, involvement assessment
CT angiography- vascular tumours, GISTS or tumouts located near major blood vessels

310
Q

Colorectal cancer: commonest type

A

adenocarcinoma

311
Q

Colorectal adenocarcinoma: histological features

A

mucinous
signet ring cell
anaplastic

312
Q

Colorectal adenocarcinoma: predisposing factors

A

ingerited polyposis syndromes
family history
chronic Crohn’s & UC
poor fruit and veg intake

313
Q

Colorectal adenocarcinoma: common location

A

left side

rectum

314
Q

Colorectal adenocarcinoma: clinical features

A
rectal &amp; sigmoid location 
- bright PR blood 
- bowel habit change
- tenesmus 
right- sided 
- iron deficiency anaemia
315
Q

Colorectal adenocarcinoma: investigations

A

PR examination
rigid sigmoidoscopy/colonoscopy
CT +/- colonography

316
Q

Colorectal adenocarcinoma: management

A
potentially curative 
-surgical resection 
- neoadjuvant chemo
- adjuvant chemo (LN involvement) 
palliative Rx
- chemo (inc. life expectancy)
- endoluminal stenting (obstructions)
317
Q

Colorectal adenocarcinoma: what is meant by potentially curative?

A

no ments
or mets curative by liver/lung resenction
technically resectable

318
Q

Colorectal adenocarcinoma right or left sided: surgical management

A

hemicolectomy

319
Q

Colorectal adenocarcinoma sigoid/rectum: surgical management

A

anterior resection

320
Q

Colorectal adenocarcinoma lower rectum: surgical management

A

low anterior resection or

adnomino-peritoneal resection

321
Q

Colorectal adenocarcinoma: staging

A
Duke's 
A- spread into muscularis propria
B- spread through full thickness bowel wall
C- lymph node involvement
D- distant mets
322
Q

Oglive’s syndrome

A

acute pseudo-obstruction (like mechanical obs. w/o cause)- > acute megacolon
seen in severely ill

323
Q

Varices prophylaxis in liver cirrhosis

A

B-blockers (propanolol)
endoscopic banding ligation
tranjugular intrahepatic porto systemic shunt (TIPS)

324
Q

Spontaneous bacterial peritonitis: associated conditions

A

commonly seen in patients with portal HTN and nephrotic syndrome

325
Q

Ileocecal valve: what is it and what is it’s function

A

sphincter muscle between small and large intestine
prevents reflux into small intestine
absorption site of B12 and bile acids