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GI Clinical 2 Flashcards

1
Q

What are the clinical signs of a small intestinal disorder?

A

Weight loss, increased appetite, diarrhoea, bloating, fatigue

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2
Q

What causes steatorrhoea?

A

Fat malaborption

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3
Q

Describe steatorrhoea

A

Pale, foul-smelling, stool less dense and floats, may leave oily marks or oil droplets

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4
Q

What minerals or vitamins may be deficient in a patient with a small intestinal disorder?

A

Iron, B12, folate, Ca2+, Mg2+, vitamin D, vitamin A, vitamin K, vitamin B complex, vitamin C

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5
Q

What is a sign of vitamin C deficiency?

A

Scurvy

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6
Q

What is a sign of deficient niacin (vitamin B complex)?

A

Dermatitis, unexplained heart failure

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7
Q

What is a sign of deficient thiamine (vitamin B complex)?

A

Memory, dementia

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8
Q

What can diseases of malabsorption (Crohn’s, coeliac) present as clinically?

A

Clubbing

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9
Q

What can finger clubbing mean clinically in the GIT?

A

Malabsorption (Crohn’s, Coeliac disease)

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10
Q

What can aphthous ulceration mean clinically in the GIT?

A

Crohn’s, Coeliac disease

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11
Q

What can be a cutaneous manifestation of coeliac disease?

A

Dermatitis herpetiformis:

Blistering, itchy (scalp, shoulders, elbows, knees)

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12
Q

What are some investigations for the structure of the GIT?

A 
Small bowel biopsy - endoscopy
Small bowel study - barium
CT scan
MRI enterography
Capsule enterography
White cell scan
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13
Q

What are tests for bacterial overgrowth in the small bowel?

A

H2 breath test

Culture a duodenal or jejunal aspirate

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14
Q

What can the H2 breath test investigate?

A

Bacterial overgrowth

Carbohydrate malabsorption e.g. lactose, glucose

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15
Q

What are the investigations for coeliac disease?

A

Serology - IgA tests (IgG if IgA deficient)
Distal duodenal biopsy
HLA status

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16
Q

What does a distal duodenal biopsy look at?

A

Villous atrophy

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17
Q

What is coeliac disease a sensitivity to?

A

Gliaden which is part of gluten (found in wheat, rye, barley)

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18
Q

What is the pathology of coeliac disease?

A

Produces inflammatory response
Partial or subtotal villous atrophy
Increased intra-epithelial lymphocytes

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19
Q

What is the gold standard diagnostic tool for coeliac disease?

A

Distal duodenal biopsy

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20
Q

What is the treatment for coeliac disease?

A

Withdraw gluten

Refer to dietician

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21
Q

What are some conditions associated with coeliac disease?

A 
Dermatitis herpetiformis
IDDM
Autoimmune thyroid disease
Autoimmune hepatitis
Primary biliary cirrhosis
Autoimmune gastritis
IgA deficiency
Downs syndrome
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22
Q

What are the complications of coeliac disease?

A 
Refractory coeliac disease
Small bowel lymphoma
Oesophageal carcinoma
Colon cancer
Small bowel adenocarcinoma
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23
Q

What are causes of malabsorption?

A

Inflammation e.g. Coeliac disease, Crohn’s
Infection e.g. tropical sprue, HIV, Giardia lamblia (parasite), Whipples’s disease
Infiltration
Impaired motility
Iatrogenic e.g. surgery
Pancreatic e.g. chronic pancreatitis, CF

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24
Q

What is giardia lamblia?

A

A parasite that causes giardiasis infection and malabsorption

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25
Q

What can giardiasis be treated with?

A

Metronidazole

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26
Q

When can small bowel bacterial overgrowth happen?

A

In any condition that affects: motility, gut structure, immunity

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27
Q

What is the treatment for small bowel bacterial overgrowth?

A

Rotating antibiotics

Vitamin and nutrient supplements

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28
Q

What are the 2 broad categories of GI disease?

A

Structural and functional

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29
Q

What is meant by a structural GI disease?

A

Detectable pathology - macroscopic/microscopic

Prognosis depends on pathology

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30
Q

What is meant by a functional GI disease?

A

No detectable pathology
Related to gut function
Long-term prognosis good

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31
Q

What are examples of functional GI disorders?

A 
Oesophageal spasm
Non-ulcer dyspepsia (NUD)
Biliary dyskinesia
IBS
Slow transit constipation
Drug related effects
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32
Q

What is non-ulcer dyspepsia?

A

Dyspeptic type pain with no ulcer on endoscopy

Probably not a single disease

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33
Q

What is the investigation process for non-ulcer dyspepsia?

A

History and examination - FH
H. pylori status
Alarm symptoms

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34
Q

What is the treatment for non-ulcer dyspepsia if all investigations are negative?

A

Treat symptomatically

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35
Q

What is the treatment for non-ulcer dyspepsia if H.pylori positive?

A

Eradication therapy

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36
Q

What are the brain components of vomiting and nausea?

A

Vomiting centre

Chemoreceptor trigger zone (CTZ)

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37
Q

If symptoms occur immediately after food, what is the likely cause?

A

Psychogenic

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38
Q

If symptoms occur 1hr+ after food, what is the likely cause?

A

Pyloric obstruction

Motility disorders e.g. diabetes, post-gastrectomy

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39
Q

If symptoms occur 12hrs after food, what is the likely cause?

A

Obstruction

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40
Q

What are possible functional GI disorder causes?

A 
Drugs
Pregnancy
Migraine
Cyclical vomiting syndrome
Alcohol
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41
Q

How does psychogenic vomiting usually present?

A

Often young women, often for years
May have no preceding nausea
May be self-induced (overlap with bulimia)
Appetite usually not disturbed but may lose weight
Often stops shortly after admission

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42
Q

What are functional diseases of the lower GIT?

A

IBS

Slow transit constipation

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43
Q

What is the average stool weight in the UK?

A

100-200g/day

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44
Q

What are the ALARM symptoms when assessing a patient?

A 
>50yo
Short symptom history
Unintentional weight loss
Nocturnal symptoms
Male
FH of bowel/ovarian cancer
Anaemia
Rectal bleeding
Recent antibiotic use
Abdominal mass
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45
Q

What investigations could you do for functional lower GIT symptoms?

A 
FBC
Blood glucose
U+E
Thyroid status
Coeliac serology
FIT testing
Sigmoidoscopy
Colonoscopy then biopsy
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46
Q

What is a FIT test?

A

Faecal immunological testing

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47
Q

What are some organic causes of constipation?

A 
Strictures
Tumours
Diverticualr disease
Proctitis
Anal fissure
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48
Q

What is proctitis?

A

Inflammation of the lining of the rectum

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49
Q

What are some functional causes of constipation?

A 
Megacolon
Idiopathic constipation
Depression
Psychosis
Institutionalised patients
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50
Q

What are some systemic causes of constipation?

A

DM
Hypothyroidism
Hypercalcaemia

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51
Q

What are some neurogenic causes of constipation?

A 
Autonomic neuropathies
Parkinson's
Strokes
MS
Spina bifida
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52
Q

What are some synonyms for IBS?

A

Nervous colon, unstable colon, spastic colon, mucous colitis - ALL inappropriate

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53
Q

What are the clinical features of IBS?

A

Abdominal pain, altered bowel habit, abdominal bloating, bleching wind and flatus, mucus

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54
Q

What is the usual pattern of IBS symptoms?

A

Chronic relapsing, remitting manner

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55
Q

What are the NICE guidelines for diagnosing IBS?

A 
Abdominal pain/discomfort relieved by defection or associated with altered stool frequency/form, plus two or more of:
Altered stool passage
Abdominal bloating/distention
Symptoms made worse by eating
Passage of mucus
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56
Q

What type of altered bowel habit might IBS patients experience?

A 
Constipation (IBS-C)
Diarrhoea (IBS-D)
Both (IBS-M)
Variability
Urgency
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57
Q

What are the investigations for IBS?

A 
Blood analysis: FBC, U+E, LFTs, Ca, CRP, TFTs, coeliac serology
Stool culture
Calprotectin
FIT testing
Rectal examination
?Colonscopy
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58
Q

What is calprotectin?

A

A protein biomarker present in faeces when intestinal inflammation occurs

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59
Q

What is calprotectin used for?

A

Differentiating between IBS and IBD and for monitoring IBD

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60
Q

Which is calprotectin present in: IBS or IBD?

A

IBD

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61
Q

What does the FODMAP diet stand for?

A

Fermentable Oligo-, Di- and Mono-Saccharides and Polyols

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62
Q

What is the FODMAP diet made up of?

A

Fructose, lactose, fructans, galactans, polyols

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63
Q

What are drug therapies for pain in IBS?

A

Antispasmodics

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64
Q

What are drug therapies for bloating in IBS?

A

Some probiotics

Linaclotide (IBS-C)

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65
Q

What are drug therapies for constipation in IBS?

A

Laxatives

Linaclotide

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66
Q

What are drug therapies for diarrhoea in IBS?

A

Antimotility agents

FODMAP

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67
Q

What are psychological interventions for IBS?

A

Relaxation training
Hyponotherapy
CBT
Psychodynamic interpersonal therapy

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68
Q

What are some causes of IBS?

A

Altered motility
Visceral hypersensitivity
Stress, anxiety, depression

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69
Q

What is the pattern of disease in IBD?

A

Chronic relapsing

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70
Q

What is the classification system for Crohn’s disease/IBD?

A

Montreal classification

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71
Q

When is the peak incidence of ulcerative colitis?

A

20-40yrs

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72
Q

Who is ulcerative colitis more common in: females or males?

A

Females

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73
Q

How does ulcerative colitis present?

A

Bloody diarrhoea, abdominal pain, weight loss

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74
Q

What are markers of a severe attack of ulcerative colitis?

A 
Stool frequency: >6/day with blood
AND
Fever >37.5
Tachycardia = >90/min
ESR(CRP) = raised
Anaemia = Hb<10g/dl
Albumin = <30g/l
Leucocytosis, thrombocytosis
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75
Q

Where does ulcerative colitis only affect?

A

Colon

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76
Q

Where does Crohn’s disease affect?

A

Mouth to anus

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77
Q

What are the clinical features of Crohn’s disease?

A

Diarrhoea, abdominal pain, weight loss, malaise, lethargy, anorexia, N+V, low-grae fever, malabsorption signs: anaemia, vitamin deficiency

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78
Q

What are some of the complications of Crohn’s disease?

A

Strictures, fistulas

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79
Q

What would test results be like for Crohn’s disease?

A 
Blood:
High ESR+CRP
High platelet count
High WCC
Low Hb
Low albumin
High calprotectin
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80
Q

What are the different values for calprotectin?

A

<50 normal
50-200 equivocal
>200 elevated

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81
Q

What specific histology would you expect with Crohn’s disease?

A

Granulomas

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82
Q

What are some extra-intestinal manifestations would you expect with IBD?

A

Eyes: uveitis, conjunctivitis
Joints: sacroilitis, ankylosing spondylitis
Renal caculi: in Crohn’s
Liver and biliary tree: gallstones, sclerosing cholangitis
Skin: erythema nodosum, vasculitits

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83
Q

What are some DDs for IBD?

A

Chronic diarroheas
Ileo-caecal TB
Different colitis’

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84
Q

What is sclerosing cholangitis?

A

Disease of the bile ducts = multiple strictures

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85
Q

What is a long-term complication of colitis?

A

Colonic carcinoma

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86
Q

Which type of ulcerates colitis is more likely to develop colonic carcinoma?

A

Pancolitis

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87
Q

After what duration of having ulcerative colitis are you more at risk of developing colonic carcinoma?

A

20yrs

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88
Q

What is 5-ASA?

A

Aminosalicylates

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89
Q

What is the medical management for outpatients with ulcerative colitis?

A

Aminosalicylates (5-ASA)
Steroids
Immunosuppression

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90
Q

What is the medical management for inpatients with ulcerative colitis?

A

Steroids
Anticoagulation
Rest

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91
Q

What is an example of an aminosalicylate?

A

Mesalazine

92
Q

What is the treatment for Crohn’s?

A 
Steroids e.g. prednisolone
Thiopurines
Methotrexate
Immunosuppressants
Biologics e.g. anti-TNFalpha antibodies
Elemental feeding
93
Q

What is the surgery for acutely ill severe colitis?

A

Total colectomy
Rectal preservation
Ileostomy

94
Q

What surgical procedure requires no ileostomy?

A

Pouch procedure

95
Q

What are bedside investigations for GI?

A 
BMI
Pulse oximetry (O2 sats)
ECG
Capillary glucose
Urinalsysis
96
Q

What investigations can you do from a stool sample?

A

FOB testing (faecal occult blood)
Stool culture
Faecal calprotectin
Faecal elastase

97
Q

What investigations can you do from a blood sample in GI?

A 
U+E
Calcium/magnesium
Liver functions tests (hepatic: high ALT, GGT, obstructive: high bilirubin, ALP)
CRP
Thyroid function
FBC: anaemia, WCC, platelet count
Coagulation (hepatic dysfunction)
Haematinics: B12, folate, ferritin
Hepatic screen: hep B/C serology, autoantibodies, immunoglobulins, ferritin, alpha-1 antitrypsin, alpha fetoprotein
Coeliac serology
Tumour markers
98
Q

What are examples of GI physiology investigations?

A

Breath testing: urea breath test (H.pylori), H+ breath test (bacterial overgrowth), lactose intolerance

Oesophageal pH and manometry: assessment for oesophageal dysmotility and assess reflux

99
Q

What can you also do whilst performing an upper GI endoscopy?

A

Biopsy

Stenting

100
Q

What are the risks with upper GI endoscopy?

A

Aspiration, perforation, haemorrhage

101
Q

What is EMR?

A

Endoscopic mucosal resection

102
Q

What can you also do whilst performing a colonoscopy/

A

Biopsy
EMR
Polypectomy

103
Q

What are the risks with colonoscopy?

A 
Haemorrhage
Renal impairment (bowel preparation - Picolax)
104
Q

What is ERCP?

A

Endoscopic retrograde cholangio-pancreatography

105
Q

What does a ERCP allow you to do?

A

Visualise ampulla, biliary system and pancreatic ducts

Biopsy/cytology, stone removal, stunting, dilatation

106
Q

What are the risks of ERCP?

A

Pancreatitis, haemorrhage, perforation, infection, mortality

107
Q

What is EUS?

A

Endoscopic ultrasound

108
Q

When is EUS used?

A

Diagnosis and staging

Allows biopsy and cyst drainage

109
Q

What is enteroscopy used for?

A

Small intestine

Biopsy/therapy for small bowel pathology

110
Q

What are the advantages and disadvantages of capsule enteroscopy?

A

Pro: less invasive
Con: no biopsy possible

111
Q

What type of pain accompanies acute pancreatitis?

A

Upper abdominal pain

112
Q

What is particularly elevated with acute pancreatitis?

A

Serum amylase

113
Q

What are the biggest causes of acute pancreatitis?

A

Alcohol abuse

Gallstones

114
Q

What are the investigations for acute pancreatitis?

A 
Blood tests: amylase/lipase, FBC, U+Es, LFTs, Ca2+, glucose, ABGs, lipids, coagulation screen
Abdominal XR
CXR
Abdominal ultrasound
CT scan
115
Q

What criteria is used to assess the criteria of acute pancreatitis?

A

Glasgow criteria

116
Q

What is the acronym for the Glasgow criteria for acute pancreatitis

A 
PANCREAS
PO2 <60mmHg
Age >55
Neutrophilia WBC >15
Calcium <2mmol/l
Renal urea >16mmol/l
Enzymes (AST >200iu/l, LDH >600iu/l)
Albumin <32g/l
Sugar glucose >10mmol/l
117
Q

When does the Glasgow criteria indicate severe pancreatitis?

A

Score >3 within 48hrs admission

118
Q

What CRP also indicates severe pancreatitis?

A

> 150mg/l CRP

119
Q

What is the management of acute pancreatitis?

A 
Analgesia (pethidine, indomethacin)
IV fluids
Blood transfusion (Hb<10g/dl)
Monitor urine output (catheter)
NG tube
Oxygen
May need insulin
Nutrition
120
Q

What is the management of pancreatic necrosis?

A

CT guided aspiration -> antibiotics +/- surgery

121
Q

What is the management in acute pancreatitis if there are gallstones?

A

EUS/MRCP/ERCP

Cholecystectomy

122
Q

What are the complications of acute pancreatitis?

A

Abcess -> antibiotics and drainage

Pseudocyst

123
Q

What is a pseudocyst in relation to acute pancreatitis?

A

Fluid collection without epithelial lining
Comes with persistent hyperamylasaemia and/or pain
Complications: jaundice, infection, haemorrhage, rupture
<6cm diameter -> resolve spontaenously
Endoscopic drainage or surgery if persistant pain or complications

124
Q

What is chronic pancreatitis?

A

Continuing inflammatory disease of the pancreas characterised by irreversible glandular destruction and typically causing pain and/or permanent loss of function

125
Q

Does chronic pancreatitis affect males or females more?

A

Males

126
Q

What is the typical age of onset of chronic pancreatitis?

A

35-50yrs

127
Q

What are the causes of chronic pancreatitis?

A 
Alcohol
Cystic fibrosis (2%) - gene mutations
Congenital anatomical abnormalities
Hereditary pancreatitis (rare; auto. dom.)
Hypercalcaemia
?Diet
128
Q

What are the most well-recognised pancreatitis-susceptibility genes?

A

PRSS1
SPINK1
CFTR

129
Q

What is the pathogenesis of chronic pancreatitis?

A

Duct obstruction: calculi, inflammation, protein plugs
?Abnormal sphincter of Oddi function: spasm/relaxation
?Genetic polymorphisms: abnormal trypsin activation

130
Q

What is the pathology of chronic pancreatitis?

A

Glandular atrophy and replacement by fibrous tissue
Ducts become dilated, tortuous and strictured
Inspissated secretions may calcify
‘Exposed’ nerves due to loss of perineural cells
Splenic, SMV and portal veins may thrombus -> portal hypertension

131
Q

What are the clinical features of chronic pancreatitis?

A 
Early disease = asymptomatic
Abdominal pain (exacerbated by food+alcohol)
Weight loss (pain, anorexia, malabsorption)
Exocrine insufficiency: fat malabsorption (steatorrhoea), protein malabsorption, decrease in fat soluble vitamins
Endocrine insufficiency (diabetes)
Jaundice, portal hypertension, GI haemorrhage, pseudocysts, ?pancreatic carcinoma
132
Q

What investigations would you do for chronic pancreatitis?

A 
Plain AXR
US
EUS
CT
Blood tests: serum amylase, albumin, Ca2+, Mg2+, vit B12, LFTs, prothrombin time, glucose
Pancreatic function tests
133
Q

What would you expect serum amylase to be in chronic pancreatitis?

A

Raised serum amylase

134
Q

What do a lot (not all) of plain AXRs show for those with chronic pancreatitis?

A

Calcification of pancreas

135
Q

What is the management for chronic pancreatitis?

A 
Avoid alcohol
Pancreatic enzyme supplements
Opiate analgesia
Coeliac plexus block (for pain)
Referral to pain clinic
Endoscopic treatment of pancreatic duct stones and strictures
Surgery
Low fat diet
Insulin (diabetes)
136
Q

What is the most common carcinoma of the pancreas?

A

Duct cell mutinous adenocarcinoma

137
Q

Which part of the pancreas is most commonly affected by carcinoma?

A

Head

138
Q

What are the clinical features of pancreatic cancer?

A 
Upper abdominal pain
Painless obstructive jaundice
Weight loss
Anorexia, fatigue, diarrhoea/steatorrhoea, nausea, vomiting
Tender subcutaneous fat nodules
Thrombophlebitis migrans
Ascites
Portal hypertension
139
Q

What are the physical signs of pancreatic cancer?

A 
Hepatomegaly
Jaundice
Abdominal mass
Abdominal tenderness
Ascites, splenomegaly
Supraclaviclar lymphadenopathy
Palpable gallbladder
140
Q

What imaging modalities could you use for pancreatic cancer?

A 
USS
CT
MRI
EUS
ERCP
Percutaenous needle biopsy
141
Q

If there is jaundice and a mass, what investigation would you do?

A

ERCP +/- stent

142
Q

If there is mass without jaundice, what investigation would you do?

A

EUS/percutaneous needle biopsy

143
Q

What is the management for pancreatic cancer?

A 
Radical surgery = pancreatoduodenectomy (Whipple's procedure)
Palliation of jaundice = stent/cholechoduodenostomy
Pain control (opiates, coeliac plexus block, radiotherapy)
144
Q

What is the radical surgery for pancreatic cancer?

A

Pancreatoduodenectomy

145
Q

What is the criteria for a pancreatoduodenoectomy?

A

Patient is fit
Tumour <3cm diameter
No metastases

146
Q

What is the mean survival for pancreatic cancer in inoperable cases?

A

<6 months

1% 5yr survival

147
Q

What is the mean 5yr survival for pancreatic cancer in operable cases?

A

15%

148
Q

How would you assess if a patient were fit for pancreatic resection?

A

Basic history and examination
CXR, ECG
Respiratory function tests
Physiological scoring system

149
Q

What is the first investigation for pancreatic cancer to see if it is resectable?

A

USS

150
Q

If it is unresectable after USS, what is the next step?

A

ERCP + stent

151
Q

What is Kausch-Whipple/Whipple surgery?

A

Pancreatoduodenectomy = due to shared blood supply often means surgical removal of head of pancreas, duodenum, proximal jejunum, gallbladder and occasionally part of the stomach

152
Q

What is PPPD surgery?

A

Pylorus preserving pancreatoduodenectomy

153
Q

How would you manage obstructive jaundice?

A

Palliative bypass

ERCP or PTC stenting

154
Q

How would you manage duodenal obstruction?

A

Palliative bypass

Duodenal stent

155
Q

How is mild acute pancreatitis classified?

A

Associated with minimal organ dysfunction and uneventful recovery

156
Q

How is severe acute pancreatitis classified?

A

Associated with organ failure or local complication

157
Q

What are local complications of acute pancreatitis?

A

Acute fluid collections
Pseudocyst
Pancreatic abscess
Pancreatic necrosis

158
Q

What is the mnemonic for remembering the causes of acute pancreatitis?

A

GET SMASHED

G = gallstones
E = ethanol (alcohol)
T = trauma
S = steroids
M = mumps (viruses)
A = autoimmune
S = scorpion bites
H = hypercalcaemia, hyporthermia, hyperlipidaemia
E = ERCP
D = drugs (azathiaprin)
159
Q

What can you use to predict how severe acute pancreatitis is?

A

Clinical assessment
Modified Glasgow criteria
CT scanning
Individual markers: CXR, CRP (>200), IL 6, TAP

160
Q

What is CT scanning useful for in acute pancreatitis?

A

Helpful to diagnose
Days 4-10 to identify necrosis
Useful for complications e.g. ascitic fluid collections, abscess, necrosis, monitoring progress of disease

161
Q

What is the mnemonic for remembering the causes of chronic pancreatitis?

A

O-A-TIGER

O = obstruction of main pancreatic duct (tumour, sphincter of Oddi dysfunction etc.)
A = autoimmune
T = toxin (alcohol, smoking, drugs)
I = idiopathic
G = genetic (auto. Dom., CF)
E = environmental (tropical chronic pancreatitis)
R = recurrent injuries (biliary, hyperlipidaemia, hypercalcaemia)
162
Q

What causes release of bile from the gallbladder

A

CKK

163
Q

What is cholesterosis?

A

Cholesterolosis occurs when there’s a buildup of cholesteryl esters and they stick to the wall of the gallbladder forming polyps

164
Q

What are gallstones made from?

A

Mixed (cholesterol and pigment)

165
Q

What is choledocholithiasis?

A

Stones in the bile ducts

166
Q

What are the symptoms and signs of obstructive jaundice?

A

Pain, jaundice, dark urine, pale stool, pruritus, steatorrhoea

167
Q

What are the clinical signs of choledocholithiasis?

A

Obstructive jaundice
Acute pancreatitis
Ascending cholangitis

168
Q

What are the investigations for gallstones?

A 
Blood tests: LFTs, amylase, lipase, WCC
USS
EUS
Oral cholecystography
CT scan
Radio isotope scan
IV cholangiography
MRCP
PTC
ERCP
169
Q

What are LFTs?

A

AST, ALT, ALP

170
Q

What are the causes of benign biliary tract disease?

A

Congenital - biliary atresia, choledochal cysts

Benign biliary stricture - iatrogenic, gallstone related, inflammatory

171
Q

What is biliary atresia?

A

One or more bile ducts is abnormally narrowed, blocked or absent

172
Q

What are choledochal cysts?

A

Congenital conditions involving cystic dilatation of bile ducts

173
Q

What is cholangiocarcinoma?

A

Malignancy of the bile ducts

174
Q

What are the risk factors for cholangiocarcinoma?

A 
> Age
PSC
Congenital cystic disease
Biliary-enteric drainage
Hepatolithiasis
Carcinigens
175
Q

What is the presentation of cholangiocarcinoma?

A

Obstructive jaundice
Itching
Non-specific symptoms

176
Q

What are the investigations for cholangiocarcinoma?

A 
Lab tests
USS
EUS
CT
MRCP
PTC
Angiography
PET
ERCP
Cholangioscopy
Cytology
177
Q

What is the management for cholangiocarcinoma?

A

Surgery: only curative option

Palliative:
Surgical bypass, stenting, palliative radiotherapy, chemotherapy, PDT, liver transplant (not standard)

178
Q

What are the common presentations of anorectal disorders?

A

Pain
Haemorrhage
Dysfunction

179
Q

What are examples of anorectal congenital abnormalities?

A

Imperforate anus
Uro-genital fissure
Hirshprung’s myenteric plexus deficiency

180
Q

What are examples of acquired anorectal abnormalities?

A 
Haemorrhoids
Fissure
Abscess
Fistula-in-ano
Ulceration
Cancer
Control of continence
181
Q

What is stapled anopexy?

A

A procedure for prolapse and haemorrhoids (PPH)

182
Q

What happens in stapled anopexy?

A

The operation pulls the swollen and prolapsing blood vessels of the haemorrhoids (piles) back into their normal position by removing a circumferential section (complete ring) of the internal rectal lining

183
Q

What is the management of anal fissures?

A

Medical - topical nitrate oxide, glyceryl trinitrate paste, diltiazem calcium blocker
Surgical - internal lateral sphincterotomy

184
Q

What is the aim of management of anal tissues?

A

Relax internal anal sphincter

185
Q

What is the management of perianal abscess?

A

Incision and drain

186
Q

Where is the most common colorectal cancer sites?

A

Left colon, then right colon

187
Q

What are the investigations for colorectal cancer?

A

Colonscopy
CT colonography
MRI guided colonscopy

188
Q

What is the treatment for anorectal cancer?

A

Anal squamous - radiotherapy

Rectal adenocarcinoma - neoadjuvant ChemoRad, laparoscopic resection

189
Q

What is a similar staging to TMN used in bowel cancer?

A

Duke’s staging

190
Q

What are causes of anal ulceration?

A

Crohn’s disease
Malignancy
Syphilis (Chancre)
Nicorandil

191
Q

What is management of control of bowel continence?

A

Sacral nerve root stimulator implant

192
Q

What are associated symptoms of constipation?

A

Headaches, nausea, loss of appetite, abdominal distention

193
Q

How do you treat secretory diarrhoea?

A

Oral rehydration therapy

194
Q

How does oral rehydration therapy treat diarrhoea?

A

Enterotoxins don’t damage villous cells, give sodium/glucose solution which drives H2O reabsorption and rehydrates, need to drink more to wash away infection

195
Q

If there are problems with the colon and rectum what do patients usually present with?

A

Change in bowel habit/continence
Bleeding
Pain
Non-intestinal manifestations

196
Q

What is visceral pain?

A

Pain receptors are in smooth muscle but pain is poorly localised

197
Q

How do the impulses run with visceral pain?

A

Afferent impulses run with sympathetic fibres accompanying segmental vessels (CP, SMA, IMA)

198
Q

What is the protocol for rectal bleeding if the symptoms are <6wks, with anal symptoms and patient is less than 40yo (low risk features)?

A

Watch and wait (6wks)

If issues after -> visualisation of large bowel

199
Q

What is the protocol for persistent change in bowel habit >6wks, persistent rectal bleeding without anal symptoms, right sided abdominal mass, palpable rectal mass, unexplained iron deficiency anaemia (high risk features)?

A

Visualisation of large bowel: colonoscopy, sigmoidoscopy +/- barium enema, CT colonography

200
Q

What are things to consider when performing colon resection/surgery?

A

Restoration of continuity
Preservation of function
Faecal diversion

201
Q

What is Hirshsprung’s disease?

A

A condition that affects the large intestine (colon) and causes problems with passing stool. The condition is present at birth (congenital) as a result of missing nerve cells in the muscles of the baby’s colon

202
Q

What are the causes of colorectal cancer?

A

Sporadic (no familial/genetic influence), familial, inheritable (HNPCC, FAP), underlying IBD

203
Q

What type of cancer are most CRCs?

A

Adenocarcinomas

204
Q

What do the majority of CRCs arise from?

A

Pre-existing polyps

205
Q

What are the main histological types of colorectal adenoma?

A

Tubular, villous, indeterminate tubulovillous

206
Q

What are the two morphological types of colorectal adenoma?

A

Pedunculated or sessile

207
Q

What leads to cell growth, proliferation and apoptosis in carcinoma?

A

Activation of oncogene
Loss of tumour suppressor gene
Defective DNA repair pathway genes (microsatellite instability)

208
Q

What is the presentation of CRC?

A

Rectal bleeding (especially mixed with stool)
Altered bowel opening to loose stools >4wks
Iron deficiency anaemia
Palpable rectal or right lower abdominal mass
Acute colonic obstruction
Systemic symptoms of malignancy: weight loss, anorexia

209
Q

What is the investigation of choice for CRC?

A

Colonoscopy (+/- biopsy, polypectomy)

210
Q

What are the risks of colonoscopy?

A

Perforation, bleeding

211
Q

What investigations can you do for CRC?

A

Colonscopy
Barium enema
CT colonography
CT abdo/pelvis

212
Q

What are the staging investigations for CRC?

A

CT chest/abdo/pelvis
MRI
PET scan/rectal endoscopic US

213
Q

What is the treatment for colorectal cancer?

A

Surgery
Chemotherapy
Radiotherapy (rectal)

214
Q

What is the prevention guidance for CRC?

A

Physical activity
Healthy BMI
Fruit and veg
No smoking

215
Q

What are the population screening methods for CRC?

A

Scottish Bowel Screening Programme

Faecal immunological testing (FIT)

216
Q

What are other screening methods for CRC?

A

Faecal occult blood test (FOBT)
Flexible sigmoidoscopy
Colonoscopy
CT colonography

217
Q

What is the Scottish Bowel Screening programme?

A

50-74yrs
FOBT every two years
FOBT+ -> colonoscopy

218
Q

Why is FOBT not always good?

A

Lower positivity in women

219
Q

What is the FIT test specific for?

A

Human haemoglobin

220
Q

What is the FIT good for which FOBT isn’t?

A

Provides flexibility to alter cut-off to accommodate risk factors including age and gender
Specific for human haemoglobin
Automated, quantative

221
Q

Which goops are high risk and are therefore screened for CRC?

A

Heritable conditions: HNPCC, FAP
IBD
Familial risk
Previous adenomas/CRC

222
Q

What is FAP (familial adenomatous polyposis)?

A

Autosomal dominant - mutation of APC gene on chromosome 5

Multiple (>100) adenomas throughout colon which have high risk of malignant change

223
Q

How are those with FAP screened?

A

Annual colonoscopy from age 10-12yrs

Prophylactic proctocolectomy usually age 16-25yrs

224
Q

What are the extracolonic manifestations of FAP?

A

Benign gastric fundic cystic hyperplastic
Duodenal adenomas in 90% with periampullary cancer
Desmoid tumours (noncancerous growths in CT)
Congenital retinal hypertrophy of the pigment epithelia (CHRPE)

225
Q

Which class of drug has been shown to reduce polyp number in FAP?

A

NSAIDs

226
Q

What is HNPCC (hereditary nonpolypsis CRC)?

A

Autosomal dominant - mutation in MMR genes
Early onset CRC right sided
Associated with endometrial, genitourinary, stomach, pancreas cancers

227
Q

Who are high risk groups of CRC?

A

Familial history CRC
IBD
Previous CRC
Previous adenomas

GI (6 decks)

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