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Gastroenterology > Lower GI > Flashcards

Lower GI Flashcards

1
Q

What is erythema multiforme?

A

A skin reaction usually mild as allergic reaction to virus or drug etc

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2
Q

What is leukoplakia?

A

Oral mucosal white patch that will not rub off and is not attributable to any other known disease

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3
Q

Fluconazole?

A

Anti-fungal medication. Eg. to treat candidiasis - orally or IV administration

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4
Q

Nystatin

A

Anti-fungal medication. Candidiasis is particularly sensitive

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5
Q

Amphotericin

A

Anti-fungal medication. Sometimes used IV for systemic fungal infections

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6
Q

Achalasia

A

Failure of oesophageal smooth muscle to relax. Aka sphincter can remain closed and fail to open when needed. Can happen throughout GIT

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7
Q

What can masses in the right iliac fossa be due to? (x11)

A 
Appendix mass/abscess 
Caecal carcinoma 
Intussusception 
Crohn's Disease 
Pelvic mass 
TB mass 
Amoebic abscess 
Actinomycosis
Transplanted kidney 
Kidney malfunction
Tumour in undescended testes
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8
Q

5 F’s of abdominal distension

A

Flatus, Fat, Fluid, Faeces, Fetus

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9
Q

2 tests to confirm ascites

A

Shifting dullness, fluid thrill/fluid wave test (pushing down prevents vibration from being transmitted through the abdominal wall)

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10
Q

Causes of ascites (without portal hypertension) x6

A

Malignancy, Infection (eg. TB), low albumin (nephrosis/nephrotic syndrome) CCF, pancreatitis, myxoedema

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11
Q

Causes of ascites with portal hypertension x4

A

Cirrhosis, Budd-Chiari syndrome, IVC or portal vein thrombosis, Portal nodes

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12
Q

4 causes of pancreatic cysts (pseudocysts)

A

Congenital, cystadenomas, retention cysts of chronic pancreatitis, cystic fibrosis.
Pseudocysts = fluid in lesser sac from acute pancreatitis

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13
Q

What are GIT synchronous tumours?

A

Two different GIT tumours at the same time

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14
Q

What are metachronous tumours?

A

Second cancer, presents months to years after first cancer but in another part of GIT

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15
Q

What met is sometimes present at presentation of colorectal cancer? What %?

A

37% have liver mets at presentation

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16
Q

Where are colorectal cancers most commonly found?

A

Sigmoid or rectum (or unspecified descending colon)

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17
Q

Typically colorectal presentation?

A

Rectal bleeding, change in bowel habits, lower abdominal discomfort, 1/2 stone weight loss

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18
Q

Left sided colorectal cancer?

A

Bleeding and mucus PR, altered bowel habit or obstruction, tenesmus, mass PR (60%)

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19
Q

Right-sided colorectal cancer?

A

Weight loss, low Hb, abdominal pain and obstruction less likely

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20
Q

What is sister mary joseph nodule?

A

Peritoneal metastasis, tumour grows out umbilicus

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21
Q

Importance of FHx in CR cancer

A

10% have FHx

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22
Q

Risk factors for CR cancer x 10

A

age (8/10 >60), male, family history, alcohol, smoking, diet (red meat, processed meat, low fibre), abdominal fatness, previous cancer, previous polyp, pre-morbidities (IBD, PSC, acromegaly)

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23
Q

Prevention of CR cancer x3

A

Aspiring >75mg/day, physical activity, foods containing dietary fibre

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24
Q

Drug treatment for CR cancer

A

Chemotherapy - usually 5-fu with oxaliplatin

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25
Q

Drugs used in palliation of advanced CR cancer

A

Bevacizumab (anti-vegF antibody), Cetuximab and Panitumumab (in KRAS wild type CR cancer - anti-EGFR agents)

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26
Q

Surgery for CR cancer x6

A 
Right hemicolectomy (for caecal, ascending or proximal transverse colon tumours)
Left hemicolectomy (for distal transverse or descending colon tumours)
Sigmoid colectomy (for sigmoid tumours)
Anterior resection of rectum (for low sigmoid or high rectal tumours) - usually no colostomy
Abdomino-perineal excision of rectum (for tumours low in rectum) - colostomy

Hartmann’s procedure - usually emergency bowel surgery - removal of sigmoid colon and/or rectum - hartmann’s because making a colostomy and leaving other end of bowel inside but closed off

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27
Q

Use of radiotherapy in CR cancer

A

Mostly palliation, occasionally pre-op to allow resection, post-op only in patients with rectal tumours at high risk of local recurrence

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28
Q

CR cancers - histologically

A

98% of colonic cancers are adenocarcinomas - from glandular epithelium

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29
Q

What do Duke stage C and D mean

A 
C = Involvement of lymph nodes 
D = distant mets
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30
Q

Indications for surgery to treat liver mets

A

Non-radiographic involvement of important vessels or lymph nodes
Complete resection must be feasible
Need enough liver left for function post-resection
No unretractable extra-hepatic sites

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31
Q

Bowel Cancer Screening

A

60-74
Home stool testing
Every 2 years
Colonscopy if positive test

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32
Q

Causes of CR cancer?

A

75% - sporadic CR cancer - isolated polyp becomes malignant
15% familial gene increases risk of polyp becoming malignant
5% hereditary non polyposis - multiple cancers run in family and increased risk of solid organ malignancies

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33
Q

Development of CR cancer

A

Lose APC protective gene and normal epithelium becomes early adenoma
Activation of promotor gene
Protective gene TP53 inactivated

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34
Q

Definition of Crohn’s

A

Chronic inflammatory GI disease characterised by transmural granulomatous inflammation affecting any part of GIT. Skip lesions (unlike UC)
Especially affects terminal ileum and proximal colon

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35
Q

Genetic mutations which increase risk of Crohn’s

A

NOD2 / CARD15

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36
Q

Prevalence and incidence of Crohn’s vs UC

A

P of C = 0.5-1/1000, P of UC 1-2/1000

I of C = 5-10/100,000/year, I of UC = 10-20/100,000/year

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37
Q

Age of presentation for Crohn’s vs UC

A

Crohn’s two peaks 20-30 years and 60-70years - worser prognosis if younger presentation
UC = 15-30

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38
Q

Associations of Crohn’s vs UC

A

Smoking = 3-4x increase risk of Crohn’s and decreases risk of UC
NSAIDs may exacerbate Crohn’s disease

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39
Q

Symptoms of Crohn’s x9

A

Diarrhoea/urgency, abdominal pain, weight loss, failure to thrive, malaise, fever, anorexia, putrid smelling stool, fluctuating symptoms

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40
Q

Signs of Crohn’s x4 GIT and x4 systemic

A

Aphthous ulcerations, abdominal tenderness/mass, perianal abscess/fistulae/skin tags, anal strictures

Skin, joint and eye problems, clubbing

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41
Q

Complications of Crohn’s x 14

A 
Small bowel obstruction 
Toxic dilatation (colon >6cm) - rarer than in UC 
Abscess formation 
Fistulae
Perforation 
Rectal haemorrhage
Colon Cancer
Fatty Liver 
PSC 
Cholangiocarcinoma 
Renal stones 
Osteomalacia
Malnutrition 
Amyloidosis
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42
Q

Stool tests - CDT and MC &S

A

CDT = c.diff toxin

MC & S = microbiology, culture and sensitivity

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43
Q

Ileal disease detection test

A

Small bowel enema

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44
Q

Signs indicative of worse Crohn’s severity x6

A 
↑ Temperature
↑ Pulse 
↑ ESR 
↑ WCC
↑ CRP 
low albumin
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45
Q

Treating a mild Crohn’s attack

A

Prednisolone PO - decrease dose if symptoms resolve

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46
Q

Treating a severe Crohn’s attack

A

NMB and IVI
Hydrocortisone IV
Metronidazole IV helps
If improving after 5 days switch to PO prednisolone
If not improving then monoclonal ab’s may help

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47
Q

Rate of surgery in Crohn’s and indications

A

50-80% need an operation in their life

I = drug failure, GI obstruction from stricture, perforation, fistulae, abscess

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48
Q

Treatment for perianal disease in Crohn’s (prevalence and x4 treatment)

A

Occurs in 50%
Oral antibiotics, immunosuppressant therapy
Local surgery +/- seton insertion

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49
Q

Definition of UC

A

Relapsing, remitting inflammatory disorder of the colonic mucosa

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50
Q

3 different types of UC

A

Proctitis - 50% - just rectum
Left-sided colitis - 30% - extends from rectum to affect part of the colon
Pancolitis - 20% - affects entire colon

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51
Q

Symptoms of UC x 6 and x2 for rectal UC

A

Diarrhoea (blood and mucus), abdominal discomfort, fever, malaise, anorexia and weight loss
Rectal UC = urgency and tenesmus

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52
Q

Acute severe UC signs x3

A

Fever, tachycardia, distended tender abdomen

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53
Q

Extraintestinal signs of UC x 15

A 
Clubbing
Aphthous oral ulcers 
Erythema nodosum 
Pyoderma gangrenosum 
Conjuncitivitis 
Episcleritis 
Iritis 
Large joint arthritis 
Sacroiliitis 
Ankylosing spondylitis
Fatty liver 
PSC 
Cholangiocarcinoma 
Nutritional deficits 
Amyloidosis
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54
Q

AXR is UC - 3 signs

A

No faecal shadows, mucosal thickening and colonic dilatation

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55
Q

Complications of UC x5

A

Perforation, bleeding, toxic dilatation of colon, venous thrombosis, colonic cancer 15% increased risk with pancolitis

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56
Q

Mild UC maintenance treatment and remission induction

A

Anti-inflammatories - 5ASA
eg. Sulfasalazine, mesalazine or olsalazine
Steroids eg. prednisolone to induce remission

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57
Q

Moderate UC remission induction

A

Prednisolone with 5-ASA and steroid enemas

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58
Q

Severe UC remission induction

A

Admit - NBM and IVI
IV hydrocortisone, rectal steroids
Transfer to prednisolone with 5asa if improving

If no improvement - may need colectomy

Or immunosuppression can be used if no remission with steroids - azathioprine, methotrexate, monoclonal ab’s

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59
Q

Surgery in UC - rates, indications and type

A

20% need it at some stage
Indications = perforation, massive haemorrhage, toxic dilatation, failed medical therapy

Proctocolectomy + terminal ileostomy

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60
Q

Side effects of 5ASA x8

A

Nausea, headache, anorexia, temperature, rash, haemolysis, hepatitis and pancreatitis

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61
Q

Maintenance therapy in Crohn’s

A

Steroid sparing agents - because patients flare up every time you take them off steroids - mainstay is Azathioprine. Also steroid sparing in UC is 5asa not working.

6mp 6mecactopurine - used for steroid dependant UC or Crohn’s

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62
Q

What are GI diverticulum and where do they occur?

A

Outpouchings of gut wall and usually at entry sites of perforating arteries

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63
Q

What is diverticulosis vs diverticular disease?

A

Presence of diverticulum vs symptomatic diverticulum

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64
Q

Where are most important/common diverticulum?

A

Colonic - sigmoid colon - where most complications occur

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65
Q

Pathology of diverticulum?

A

Lack of dietary fibre causes high intraluminal pressure - forces mucosa to herniate through muscle wall

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66
Q

How common are diverticulum?

A

30% of westerners by age 65

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67
Q

Symptoms of diverticulum?

A

Many are asymptomatic - can have bleeding, altered bowel habit, colic, nausea and flatulence

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68
Q

Symptoms of diverticulitis?

A

Same as diverticulum (nausea, colic, altered bowel habit, flatulence, bleeding) but also pyrexia, raised WCC and CRP and tender colon/localised peritonitis

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69
Q

Treatment of diverticulitis?

A

Bowel rest (fluid only- may be only treatment if mild), antibiotics if needed, analgesia, surgery not for abscesses but yes for peritonitis

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70
Q

Indications for elective surgery in diverticulitis?

A

Stenosis, fistula or recurrent bleeding

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71
Q

Signs of perforation in diverticulitis?

A

Ileus, peritonitis, shock

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72
Q

Management of haemorrhage in diverticulitis?

A

Usually just bed rest and it will stop - if bad may need surgery - diathermy can prevent need for this

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73
Q

Signs of abscesses in diverticulitis?

Treatment?

A

Swinging fever, leucocytosis, localising signs (eg. Mass)

Treatment = antibiotics - CT/US guided drainage may be needed

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74
Q

What is angiodysplasia?

A

Submucosal arteriovenous malformations that typically presents as fresh PR bleeding in the elderly - cause unknown

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75
Q

Where does angiodysplasia occur?

A

Can affect anywhere in the GI tract but 70-90% of lesions occur in right colon

76
Q

What is good for diagnosis of angiodysplasia?

A

Mesenteric angiography - shows early filling at site and then extravasation

77
Q

Treatment of angiodysplasia

A

Embolisation, endoscopic laser electro coagulation, resection

78
Q

What is a hernia?

A

Protrusion of a viscus through a defect of the walls of its containing cavity into an abnormal position

79
Q

What is an incarcerated hernia?

A

Contents of hernial sac are stuck inside by adhesions

80
Q

What is a strangulated hernia?

A

One where ischaemia occurs

81
Q

Indirect vs direct inguinal hernia

A

Indirect - through internal inguinal ring. Direct - through abdominal wall through posterior wall of inguinal canal

82
Q

What is defect in abdominal wall called and what are its boundaries?

A

Hesselbach triangle - laterally - inferior epigastric artery, medially - rectus abdominis, inferiorly - inguinal ligament

83
Q

Risk factors for inguinal hernia x7

A

Male (8:1), chronic cough, constipation, urinary obstruction, heavy lifting, ascites, previous abdominal surgery

84
Q

Differentiating direct from indirect

A

Gold standard is surgically - direct are lateral to inferior epigastric vessels and indirect arise medially

85
Q

Direct vs indirect - which is more common?
Which strangulates more?
Which is more
Often reducible?

A

Indirect more common 80%
Direct reduce more easily
Indirect strangulate more easily

86
Q

Repairs of hernia x2

A

Polypropylene mesh to reinforce posterior wall. Laparoscopic repair

87
Q

Where do femoral hernias appear?

A

Mass in upper medial thigh or above inguinal ligament (points down the leg as opposed to inguinal pointing to the groin)

88
Q

3 features of femoral hernias

A

More common in women, irreducible and strangulate easily due to rigidity of canal borders

89
Q

Boundaries of femoral canal

A

Anteriorly - inguinal ligament, medially - lacunar ligament and pubic bone, laterally - femoral vein, posteriorly - pectineal ligament and pectineus

90
Q

DDX of femoral hernia x6

A

Inguinal hernia, saphena varix, enlarged cloquets node, lipoma, femoral aneurysm, psoas abscess

91
Q

Risk factors for paraumbilical hernia x2

A

Obesity and ascites

92
Q

Where do epigastric hernias go?

A

Through linea alba above umbilicus

93
Q

What is gastroschisis?

A

Congenital defect causing protrusion of abdominal contents through a defect in the anterior abdominal wall

94
Q

Definition of IBS

A

Mixed group of abdominal symptoms for which no organic cause can be found

95
Q

Prevalence of IBS, age at onset and F:M ratio

A

10-20% (probably higher)

96
Q

Features required for IBS diagnosis

A

1) Abdominal pain/discomfort is relieved by defecation
OR
2) Altered stool or bowel frequency - constipation and diarrhoea alternate

Plus >2 of 
Urgency
Incomplete evacuation 
Abdominal bloating/distention 
Mucus PR 
Worsening of symptoms after food

DIAGNOSIS OF EXCLUSION

97
Q

Other symptoms present in IBS

A 
Nausea
Bladder symptoms
Chronic >6months 
Backache 
Exacerbated by stress, menstruation or gastroenteritis
98
Q

Treatment of IBS

A 
Rarely successful 
Just make symptoms less intrusive 
Things which may worsen disease:
- Fibre
- Lactose
- Fructose
- Wheat
- Starch 
- Caffeine 
- Sorbitol 
- Alcohol 
- Fizzy drinks
99
Q

Management of IBS if constipation

A

High fibre can make worse
Avoid insoluble fibre
Bisacodyl and sodium picosulfate can make better
Ispaghula has non-fermentable water-soluble fibre

100
Q

Management of IBS if diarrhoea

A

Avoid sorbitol sweeteners

Try bulking agent +/- loperamide after each loose stool

101
Q

Management of IBS if colic/bloating

A

Oral antispasmodics

Active bacillus

102
Q

Symptoms of gastrointestinal malabsorption

A 
Diarrhoea
Weight Loss 
Lethargy 
Steatorrhoea (hard to flush away)
Bloating
103
Q

Signs of deficiencies due to GI malabsorption

A 
Anaemia (Iron, folate and B12)
Bleeding disorders (vitamin K)
Oedema (protein)
Metabolic bone disease (vitamin D)
Neurological features
104
Q

Tests in GI malabsorption

A

Bloods - low b12, folate, iron, calcium

Stool - fat globules (Sudan stain), microscopy (infestation)

Barium-follow through (Diverticula, crohns)

Breath hydrogen (bacterial overgrowth)

ERCP - pancreatitis, biliary obstruction

105
Q

Common causes of GI malabsorption in UK

A

Coeliac disease
Chronic pancreatitis
Crohn’s disease

106
Q

Rarer causes of GI malabsorption

A

PBC
Ileal resection
Biliary obstruction

Pancreatic cancer
CF

Tropical disease

Surgery to have removed part of digestive system

107
Q

What is Coeliac’s disease

A

T-cell mediated autoimmune disease of small bowel

Where prolamin intolerance (in wheat etc) causes villous atrophy and malabsorption

108
Q

When do you suspect Coeliacs?

A

All with diarrhoea, weight loss and anaemia

109
Q

Prevalence of Coeliacs

A

1 in 300-1500
More common in the Irish

Peaks in infancy and 50-60 years

110
Q

Associations of Coeliacs

A

Familial component

HLA DQ2 in 95% (rest are DQ8)

111
Q

Presentation of Coeliacs

A

Stinking stools/steartorrhea
Diarrhoea

Abdominal pain
Bloating
N and v

Weight loss
Fatigue and weakness

Aphthous ulcers
Angular somatitis

Osteomalacia
Easy bruising
Children fail to thrive (wasted buttocks)

112
Q

Diagnosis of Coeliacs - blood test

A

Low Hb and ferritin
RCDW increase
Low B12

113
Q

Antibodies in Coeliacs

A

IgG Anti-gliadin

IgA, IgG Anti-endomysial transglutaminase

114
Q

Last diagnosis for Coeliacs

A

Biopsy at endoscopy
Shows subtotal villous atrophy
Raised intraepithelial WBCs

Features reverse on gluten-free diet

115
Q

Treatment of Coeliacs

A

Life-long gluten free diet

Rice, maize, soya, potatoes, oats and sugar are okay

116
Q

Complications of Coeliacs

A

Anaemia
Secondary lactose-intolerance

GI T-cell lymphoma

Increase risk of other malignancy (gastric, oesophageal, bladder, breast, brain)

Myopathies
Neuropathies

Hyposplenism

Osteoporosis

117
Q

Digestion of carbohydrates

A

Starch breakdown - starts in mouth but most occurs under action of pancreatic amylase in upper intestine - sugars!!

118
Q

Digestion of protein

A

Pancreatic proteolytic enzymes into amino acids and peptides - occurs in duodenum

119
Q

Digestion of fat

A

Digestion by bile and pancreatic lipase in duodenum

Bile salts absorbed in terminal ileum

120
Q

Water and electrolyte absorption

A

Upper jejunum - ileum - colon

121
Q

Water soluble vitamins

A

Small intestine, vitamin B12 and bile salts - terminal ileum

122
Q

Treatment of pruritus ani?

A

Careful hygiene
Moist wipe post-defecation

No spicy food

Anaesthetic cream
No steroid/antibiotic cream

123
Q

What is an anal fissure?

A

Painful tear in squamous lining of lower anal canal

124
Q

Where are anal fissures usually located?

A

90% are posterior

125
Q

Causes of anal fissure

A

Most are due to hard faeces

Spasm may constrict inferior rectal artery - causing ischaemia - making healing difficult and perpetuating the problem

126
Q

Other rare causes of anal fissure

A

Syphilis, herpes, trauma, crohn’s, anal cancer and psoriasis

127
Q

Medical treatment of anal fissure

A

5% lidocaine ointment
GTN ointment

Topical diltiazem (calcium channel blocker)
Botox injections
128
Q

Conservative treatment of anal fissure

A

Increase dietary fibre
Fluids + stool softener
Hygiene advice

129
Q

What is anal fistula? How arise pathologically?

A

Track communicates between skin and anal canal/rectum

Blockage of deep intramuscular glands thought to predispose to formation of abscesses - this discharge to the skin to form fistulas

130
Q

Symptoms of anal fistula

A

Pain and irritation

131
Q

Causes of anal fistula

A

Perianal sepsis
TB
Abscesses

Crohn’s disease
Diverticular disease
Rectal carcinoma

132
Q

Tests in anal fistula

A

MRI

Endoanal US scan

133
Q

Treatment of anal fistula

A

Fistulotomy and excision

134
Q

What needs to happen in excision of a high fistula?

A

Continence of muscles of anus affected therefore ‘seton suture’ needed - tightened over time to maintain continence

135
Q

What usually causes anorectal abscesses?

A

Normally gut organisms

136
Q

Treatment of anorectal abscess

A

Incise and drain under GA

137
Q

Associations of anorectal abscess

A

DM
Crohn’s
Malignancy
Fistulae

138
Q

What is a perianal haematoma, what does it look like and how treated?

A

Thrombosed external pile. 2-4mm ‘dark blueberry’ under skin at anal margin

Can be evacuated under LA or left to resolve spontaneously

139
Q

What is pilonidal cyst?

A

Ingrowing hair 6cm above anus - causes foreign body reaction - foul-smelling discharge

M:F = 10:1

More common in obese caucasians and people from Asia, Middle East and Mediterranean (more bodily hair)

140
Q

Treatment of pilonidal cyst

A

Excision of sinus tract +/- primary closure

Ab’s pre op

141
Q

What happens in rectal prolapse?

A

Mucosa - partial/type 1
Or all layers - complete/type 2 (more common)
protrude through the anus

Incontinence in 75%

Descent of >3cm when asked to strain

142
Q

Causes of rectal prolapse

A

Lax sphincter, prolonged straining

Also related to chronic neurological disease

143
Q

Treatment of rectal prolapse - 2 approachs

A

1) Abdominal approach
- Fix rectum to sacrum (rectopexy) +/- mesh insertion +/- rectosigmoidectomy (prolapsed bit removed and two ends joined up) = Altemeier’s procedure

2) Perineal approach = Delorme’s procedure - resect mucosa close to the dentate line - push muscle back up and suture mucosal boundaries - mucosa excess stitched back to cover repair
- Anal encirclement with a Thiersch wire

144
Q

Treatment of anal warts?

A

imiquimod and podophyllotoxin

145
Q

What is Proctalgia fugax?

A

Idiopathic, intense brief stabbing, crampy rectal pain
Often worse at night
Mainstay treatment is reassurance

146
Q

How do you test muscular and sensory innervation?

A

Anocutaneous reflex - lightly stroking anal skin - sphincter should contract briefly

147
Q

Risk factors for anal cancer?

A

Syphilis
Anal warts
Anoreceptive homosexuals

148
Q

What sort of cancer is anal cancer normally?

A

Squamous cell - 85%

149
Q

When are anal canal tumours associated with poor prognosis?

A

If spread above dentate line
Poorly differentiated
Non-keratinizing

150
Q

Where does anal cancer spread to?

A

Above dentate line - to pelvic lymph nodes

Below dentate line - to inguinal lymph nodes

151
Q

Presentation of anal cancer

A 
Bleeding
Pain
Altered bowel habit
Pruritus ani 
Masses/stricture
152
Q

Treatment of anal cancer

A

Chemo-irradiation - usually preferable to anorectal excision & colostomy

153
Q

Prognosis of anal cancer

A

75% retain normal anal function

154
Q

What are piles/haemorrhoids?

A

Anus is lined by spongy vascular tissue = anal cushions - where 3 major arteries feed the vascular plexuses and enter the anal canal

These contribute to anal closure
Piles is when they get disrupted and dilated

155
Q

What causes the cushions to form piles?

A

Effects of gravity
Increased anal tone
Straining at stool - constipation

All cause them to become bulky and loose and then they protrude

156
Q

Why called haemorrhoids?

A

Because they bleed readily from the capillaries underlying

Bright red blood because from capillaries

157
Q

Are haemorrhoids painful?

A

No because there are no sensory fibres

But can thrombose when protrude if they are gripped by the anal sphincter as this blocks venous return = painful

158
Q

Classification of piles

A

1st degree - remain in rectum

2nd degree - prolapse through anus on defecation but spontaneously reduce

3rd degree - same as 2nd but require digital reduction

4th degree - persistently prolapsed

159
Q

Difference between external and internal haemorrhoid

A

External - origin below dentate line (ex.rectal plexus)

Internal - origin above dentate line (int.rectal plexus)

160
Q

Symptoms of piles

A

Bright red rectal bleeding

May be mucous discharge and pruritus ani

Severe anaemia can occur

161
Q

Medical treatment of piles - when and what? x4

A 
For 1st degree
Increase fluid and fibre 
Topical analgesics 
Stool softener 
Topical steroids for a short period
162
Q

Non-operative treatment of piles - when and what? x4

A

For 2nd and 3rd degree

1) Rubber band ligation - produces an ulcer therefore bleeding pain and infection are SE’s
- lowest recurrence rate

2) Sclerosants - 2ml of 5% phenol in almond oil injected into pile
- recurrence higher
- SE: impotence, prostatitis

3) Infra-red coagulation
- as successful as banding and might be less painful

4) Cryotherapy
- Not recommended as high complication rate

163
Q

Surgical treatment of piles - when and what? x2

A

For 4th degree piles

1) Excisional haemorrhoidectomy
- Most effective
- Excision of piles and ligation of vascular pedicles
- Day-case surgery

2) Stapled haemorrhoidectomy
- Less pain maybe
- When there is a large internal component
- Higher recurrence rate

164
Q

Treatment of prolapsed thrombosed piles

A

Analgesia, ice packs and stool softeners
Pain usually resolves in 2-3 weeks
Some say surgery

165
Q

What is dermatitis herpetiformis

A

Intense, itchy blisters seen on elbows, knees or buttocks

Skin condition linked to coeliacs

166
Q

Tumour markers in CR cancer

A

CEA (used to monitor disease progression and Ca 19-9

167
Q

Type of surgery for CR cancer in caecum, ascending colon, proximal transverse colon

A

Right hemicolectomy

168
Q

Type of surgery for CR cancer in distal transverse colon, descending colon

A

Left hemicolectomy

169
Q

Type of surgery for CR cancer in sigmoid colon

A

Sigmoid colectomy

170
Q

Type of surgery for CR cancer in high rectum

A

Anterior resection

171
Q

Type of surgery for CR cancer in low rectum

A

Abdo-perineal resection and end colostomy formation

172
Q

What is Duke Stage B

A

CR cancer staging

Breached serosa but negative lymph nodes

173
Q

What is Duke Stage A

A

CR cancer confined to bowel wall

174
Q

Investigation features of Crohns

A

Cobblestone mucosa
rose-thorn fissures
Barium showing fissures or strictures (string sign of kantor)

175
Q

What is ischaemic colitis?

A

Ischaemia of the colon due to decreased colonic blood supply which can lead to muscosal inflammation, oedema, necrosis and ulceration

176
Q

Where is most commonly affected by ischaemic colitis

A

Splenic flexure - watershed between superior and inferior mesenteric arteries

177
Q

Cause of ischaemic colitis normally

A

Occlusion of large vessels by thrombosis/embolism

therefore increased risk with atherosclerosis and AF

178
Q

Cause of ischaemic colitis in young patients

A

Small vessel vasculitis
Vasospasm (cocaine)
Hypercoagulable states

179
Q

Symptoms of ischaemic colitis

A

Can be acute or chronic in onset
Crampy abdominal pain, may be post-prandial ‘gut claudication’ therefore ‘food fear’
Fever, nausea, bloody diarrhoea

180
Q

Signs of ischaemic colitis

A 
Abdominal distention and tenderness
Local peritonism (worse on left)
Fever and tachycardia depending on severity
181
Q

Blood in ischaemic colitis

A

Raised LDH, lactate and CK

182
Q

Imaging signs in ischaemic colitis

A

Thickening of wall, intramural air - thumbprinting (submucosal oedema)

183
Q

Management of ischaemic colitis

A

Supportive, NBM and surgery if necrosis or perforated bowel

184
Q

What is pseudomembranous colitis

A

Large bowel inflammation with mucosal destruction and inflammatory exudates forming pseudomembranes on bowel wall - due to toxin releasing C-Diff

185
Q

Features of pseudomembranous colitis

A

Recent antibiotic therapy
Watery diarrhoea, may become bloody with crampy abdominal pain
Pyrexia and abdominal tenderness
Treat with metronidazole and vancomycin

186
Q

Faecal test for UC

A

Faecal calprotectin (marker for disease severity)

187
Q

Barium enema signs with UC

A

Loss of haustral pattern - leadpipe or hosepipe appearance

Gastroenterology (5 decks)

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