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Gastro Flashcards

1
Q

Common causes of GI bleed?

A 
Chronic/acute peptic ulcer
Drugs 
Mallory-Weiss
Varices
Gastric erosions
Erosive oesophagitis
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2
Q

Bloods in GI bleed?

A

FBC, U+E, LFT, amylase, glucose, clotting

Urea raised due to increased protein load

G+S if low risk, X-match if high risk

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3
Q

Investigations besides bloods in upper GI bleed?

A

Erect CXR/ECG

OGD - identification of cause and permits treatment

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4
Q

What does Glasgow Blatchford Score assess?

A

Assesses likelihood that patient will need transfusion or endoscopic intervention.

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5
Q

Results and management from GBS?

A

0/1 and stable - LOW RISK - discharge with O/P OGD or discuss with gastro reg

> 2 and stable - INTERMEDIATE RISK - discuss with reg and routine OGD (24 hours)

> 2 and unstable or varices suspetred - HIGH RISK - urgent review by gastro reg and emergency OGD

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6
Q

What does Rockall Score assess?

A

Identifies patients at risk of adverse outcome following GI bleed

Contains diagnosis (MW, malignancy etc) so can assess outcome

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7
Q

Results of Rockall score?

A

<3 = good prognosis, low risk of mortality/rebleeding

> 8 = high risk of mortality, high risk of mortality/rebleeding

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8
Q

What can you give in variceal bleed?

A

Terlipressin

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9
Q

Constipation + rectal bleeding = ?

Constipation + distenstion + active BS = ?

Constipation + menorrhagia = ?

A
  1. cancer
  2. stricture/GI obstruction
  3. hypothyroidism
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10
Q

Mnemonic for causes of constipation?

A

OPENED IT

Obstruction, pain, endocrine, neuro, elderly, diet/dehydration, IBS, toxins

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11
Q

Cause of chronic constipation in kids?

A

Hirschsprung’s

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12
Q

Investigations for constipation in elderly?

A

Bloods - exclude metabolic causes (hypothyroid, hypercalcaemia)

Review drug history

Sigmoidoscopy/barium enema to exclude cancer or diverticulitis

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13
Q

Name a bulk forming laxative and how they work?

A

Bran powder, fybogel (ispaghula husk), methylcellulose, sterculia granules

↑Faecal mass –> stimulate peristalsis – must be taken with plenty of fluid and take a few days to act.

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14
Q

Name a softener laxative and when you use them?

A

Liquid paraffin, arachis oil, sodium docusate (also has a simulant action)

Useful when managing painful anal conditions (fissure)

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15
Q

Name an osomotic laxative and how they work and side effects?

A

Lactulose, macrogol (movicol)

Retain fluid in the bowel

SE = bloating

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16
Q

Name stimulant laxatives and how they work and side effects?

A

Bisacodyl, senna (pure stimulant)
Docusate sodium, danthron (stimulant and softening)

Increase intestinal motility, so don’t use in obstruction or acute colitis. Avoid prolonged use as may cause colonic atony and hypokalaemia.

SEs = abdominal cramps

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17
Q

What can you do for rapid bowel evacuation prior to procedures?

A

Phosphate enema

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18
Q

Bloods in diarrhoea?

A

FBC - ↓MCV/Fe deficiency (coeliac/colon ca), ↑MCV if alcohol abuse or ↓B12 absorption (coeliac/Crohn’s)

ESR/CRP - Raised in infection, Crohn’s/UC, cancer

U+E - ↓K+ = severe D+V

TFTs - ?hyper

Coeliac serology

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19
Q

Investigations in diarrhoea?

A

Bloods

Stool MC+S

Rigig sigmoidoscopy + biopsy (Crohn’s)

Colonoscopy/barium enema - ?malignancy ?colitis

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20
Q

General management of diarrhoea?

A

Treat Causes

Food handlers – no work until stool samples are -ve. If hospital outbreak, isolation/ward closure may be necessary.

Avoid abx unless infective diarrhoea causing systemic upset.

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21
Q

Rehydration in diarrhoea?

A

Oral rehydration better than IV, but if impossible –> 0.9% saline + 20mmol K+/L IV.

ORS in children

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22
Q

Anitmotility agents in diarrhoea?

A

Codeine phosphate 30mg TDS PO or loperamide 2mg PO after each loose stool (max 16mg/day) –> ↓stool frequency

Avoid in colitis (may precipitate toxic megacolon)

Little evidence to suggest their use in acute diarrhoea increases risk of colonic dilatation

Should not be given to children

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23
Q

Risk factors and treatment of C.diff?

A

> 70 yrs, past C.diff infection, use of antiperistaltic drugs

Stop abx. Treatment not usually needed. Metronidazole or vanc 10 days if severe.

Complication –> toxic megacolon

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24
Q

Screening tool for malnutrition?

A

MUST (Malnutrition universal screening tool)

BMI score
Weight loss score
Acute disease effect score

0 = low risk
1 = medium risk
2 = high risk
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25
Q

Biochemical features of refeeding syndrome?

A

Fluid-balance abnormalities

Abnormal glucose metabolism (low insulin requirement –> high insulin requirement)

Hypophosphataemia

Hypomagnesaemia

Hypokalaemia

Thiamine deficiency

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26
Q

Prevention of refeeding syndrome?

A

Start refeeding at no more than 50% of energy requirements in “patients who have eaten little or nothing for more than five days”

Oral, enteral or intravenous (IV) supplements of potassium, phosphate, calcium and magnesium should be given unless blood levels are high before refeeding

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27
Q

What is Marasmus and Kwashiorkor?

A

M = Inadequate energy intake in all forms

K = Protein deficiency with adequate energy intake

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28
Q

What are anthropometric measures?

A

Body weight

Triceps skin-fold thickness

Mid-arm muscle circumference

Plasma albumin with or without transferrin and pre-albumin

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29
Q

3 general causes of GORD?

A

Raised intra-abdominal pressure

Faulty oesophageal sphincter

Drugs

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30
Q

What are the ALARMS symptoms

A 
Anaemia (iron deficiency)
Loss of weight
Anorexia
Recent onset/progression
Melena/haematemesis
Swallowing difficulty
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31
Q

Complications of GORD?

A

Oesophagitis
Ulcers
Benign stricture
Iron deficiency

Barrett’s (squamous –> columnar)

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32
Q

Investigations in GORD?

A

Endoscopy - usually normal

Barium studies

24 hour oesophageal pH monitoring (GORD = acid in oesophagus >4% of day)

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33
Q

Where does oesophageal cancer tend to arise?

A 
SCC = upper 2/3
Adeno = lower 1/3

Tumours tend to arise in areas of partial narrowing
• Pharyngo-oesophageal junction (40%)
• Junction of upper and middle 1/3 (40%)
• Where oesophagus passes through diaphragm (20%)

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34
Q

Spread of oesophageal Ca?

A

Can be locally invasive too

liver, lungs, brain, bones

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35
Q

Curative treatments for oesophageal Ca?

A

Surgical treatment – open oesophagectomy/minimally invasive oesophagectomy

Neo-adjuvant chemo-radiotherapy

Definitive chemo-radiotherapy

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36
Q

Palliation in oesophageal ca?

A

Endoscopic stenting

Brachytherapy

Chemotherapy/external radiotherapy

Feeding through gastrostomy, jejunostomy or IV

Pain relief

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37
Q

Types of hiatus hernia?

A

Sliding/Axial - direct herniation through oesophageal hiatus

Paraoesophageal/rolling - organ pushing up beside oesophagus

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38
Q

Causes of hiatus hernia?

A

Increased intraabdominal pressure –> Large ovarian cysts, pregnancy, obesity

Oesophageal shortening –> Oesophageal spasm and fibrosis from reflux – accentuated by excessive swallowing

Widening of diaphragmatic hiatus –> Muscular degeneration – around lower end of oesophagus and fundus of stomach

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39
Q

Diagnosis of hiatus hernia on endoscopy?

A

Diagnosed when the distance between diaphragmatic indentation and the squamocolumnar junction is greater than 2cm

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40
Q

Aetiology of duodenal ulcers?

A

4x more common in men – 30-50 years

Strong genetic influence – 3x more common if 1st degree relative

H.pylori infection in 95% of patients

Smoking is a risk factor

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41
Q

Aetiology of gastric ulcers?

A

2x more common in men – common in late middle age

NSAIDs – 3/4 fold increase in risk

Less related to H.pylori than duodenal – 70% of patients

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42
Q

Pain of duodenal ulcers?

A

Epigastric – onset 2-3 hours after eating

Relieved by eating and drinking milk

Radiates to back, often worse at night

Precipitating factors = missing a meal, anxiety or stress

Lasts for 1 to 2 months and occurs in 4 to 6 month cycles

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43
Q

Pain of gastric ulcers?

A

Epigastric pain – 15-30 mins after eating

Relieved by vomiting and worsened by eating

Pain often worse during the day

Lasts for a period of 2 weeks and occurs in cycles of 1-2 months

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44
Q

Presentation of perforated PU?

A

Severe, constant, sudden onset epigastric pain – may be hematemesis.

Patient looks ill, usually still, in pain, tachycardia, shallow respiration

Abdomen is flat, very tender (intense guarding) – if air has escaped into peritoneal cavity then liver dullness may be absent.

Peptic ulcer perforation results in a chemical peritonitis rather than a bacterial peritonitis in the initial stages (unlike bowel perforation)

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45
Q

Testing for H/Pylori?

A

Carbon-13 urea breath test
OR
Stool antigen test

Production of radiolabelled CO2 from swallowed urea – most accurate test. If urease (enzyme that uses H.pylori to metabolise urea) is present, H.pylori is present.

Need to have not taken PPI or abx in past 4 weeks

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46
Q

Imaging for peptic ulcer?

A

Endoscopy

Gastric ulcer should be biopsied (?malignancy) – further endoscopy after treatment to ensure healing.

Duodenal ulcer - not necessary to biopsy – follow up endoscopy is not required if patient has become asymptomatic

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47
Q

3 steps for treating H pylori?

A

Step A = lifestyle changes

Step B = H.pylori testing

Step C = Eradication therapy

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48
Q

Step B (H.pylori testing) of peptic ulcer treatment?

A

If +ve and associated with NSAID use –> full dose PPI for 2 months then step C

If +ve and not associated with NSAID use –> step C

If –ve –> full dose PPI for 1-2 months

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49
Q

Eradication therapy for H.Pylori?

A

7 day, twice-daily course of
o A PPI
o Amoxicillin 1g
o Clarithromycin 500mg or Metronidazole 400mg

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50
Q

Metabolic abnormaliites in coeliac disease?

A

Iron/folate deficiency, vitamin K deficiency, vitamin D deficiency and hypocalcaemia

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51
Q

Skin sign in coeliac?

A

Dermatitis herpetiformis

60-80% - intensely itchy blisterning rash on trunk and extensor surfaces of limbs

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52
Q

Bloods in coeliac?

A

Anti-TTG

FBC (anaemia)

LFTs (elevated transminases)

B12, folate, ferritin, calcium

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53
Q

Definitive diagnosis of coelic?

A

Jejunal biopsy (endoscopic)

Must be on gluten diet until biopsy (villi return to normal on gluten-free)
Will show subtotal villous atrophy

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54
Q

Signs in acute pancreatitis?

A

Fever, hypotension, tachycardia, tachypnea, or diaphoresis

Epigastric tenderness, with guarding on abdominal examination

Decreased bowel sounds

Jaundice - suggests choledochal obstruction from gallstone pancreatitis

Grey-Turner’s sign - ecchymosis of the flank and Cullen sign - ecchymoses in the periumbilical region

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55
Q

Local complications of acute pancreatitis?

A

Acute pancreatic fluid collection (first 4 weeks)

Pancreatic pseudocyst (after 4 weeks)

Acute necrotic collection (first 4 weeks)

Walled off necrosis (after 4 weeks)

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56
Q

Systemic complications of acute pancreatitis

A

Circulatory shock (kinin activation, haemorhage)

DIC

Respiratory insufficiency (hypoxaemia, atelectasis, pleurak effusion, ARDS)

Acute renal failure

Metabolic (hypocalcaemia, hyperglycaemia/DM, hypertriglyceridaemia)

Pancreatic encephalopathy (confusion, delusions, coma)

Retinal arteriolar obstruction (sudden blindness)

Metastatic fat necrosis

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57
Q

Diagnostic criteria for acute pancreatitis

A

ATLANTA CLASSIFICATION

  1. Abdominal pain - acute onset of a persistent, severe, epigastric pain often radiating to the back)
  2. Serum lipase activity (or amylase activity – lipase more sensitive) at least three times greater than the upper limit of normal
  3. CECT - Characteristic findings of acute pancreatitis on contrast-enhanced CT

(CT not usually required)

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58
Q

Bloods in acute pancreatitis?

A

FBC - leucocytosis/raised Hb due to haemoconcentration

U+E. LFTs – elevated liver enzymes –> gallstones probably cause

Triglyceride, calcium, LDH, CRP levels

ABG

Urinalysis

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59
Q

Imaging in acute pancreatitis?

A

Abdo USS - look for gallstones

Erect CXR - rule out perf DU

AXR - may show ground glass appearance due to presence of peritoneal exudate. Bowel gas usually absent apart from central dilated section of duodenum/jejunum (‘sentinel’ loop) - indicates localised ileus

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60
Q

What is the Glasgow criteria?

A

Valid for gallstone and alcohol induced pancreatitis –> 3 or more needs ICU

P - PaO2 <8kPa
A - Age >55-years-old
N - Neutrophilia: WCC >15x10(9)/L
C - Calcium <2 mmol/L	
R - Renal function: Urea >16 mmol/L
E - Enzymes: LDH >600iu/L; AST >200iu/L
A - Albumin <32g/L (serum)
S - Sugar: blood glucose >10 mmol/L
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61
Q

Management of acute pancreatitis

A

Fluid resuscitation and oxygen supplementation

Analgesia (opioids - improves respiratory function)

Nutritional support (if no N+V and no pain, can start eating. If severe enteral feeding recommended)

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62
Q

Surgical management in acute pancreatitis?

A

ERCP
If existing cholangitis or biliary obstruction

Cholecystectomy
For gallstones – after initial symptoms have resolved.

Percutaneous aspiration or Surgical debridement
For patients with severe pancreatitis and infected necrosis or persistent fluid collections

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63
Q

Subsequent things in acute pancreatitis?

A

May affect pancreatic endocrine function –> hyperglycaemia (needs monitoring)

May need pancreatic enzyme supplements

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64
Q

Contents of the spermatic cord?

A

External/internal spermatic and creamasteric fascia

Spermatic cord
o Vas, obliterated processus vaginalis, vasculature, pampiniform plexus, genital branch of genitofemoral nerve + sympathetic nerves

Ilioinguinal nerve

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65
Q

What is an indirect inguinal hernia?

A

Originate lateral to inferior epigastric artery.

Pass through internal inguinal ring along inguinal canal and, if large, out through the external ring

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66
Q

What is a direct inguinal hernia?

A

Originate medial to inferior epigastric artery.

Push their way directly through a weakness the posterior wall of the inguinal canal (Hesselbach’s triangle)

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67
Q

What is a congenital inguinal hernia?

A

Results from a patent processus vaginalis. Can be large enough to allow abdominal or pelvic organs to descend.

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68
Q

What happens in a strangulated inguinal hernia?

A

Most commonly occurs at external inguinal ring. Most commonly in elderly and in first 6 months of life.

  • Constriction of the hernial neck, or twisting of the hernia, initially obstructs venous return
  • Oedema eventually obstructs arterial supply
  • Eventually the bowel necroses and perforates into the hernial sac
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69
Q

Symptoms of an inguinal hernia?

A

Discomfort/pain in groin

Lump/mass in scrotum (can be reducible)

Abdo pain (if colicky –> obstruction)

Vomiting, abdominal distension, absolute constipation (obstruction)

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70
Q

What would irreducibility of an inguinal hernia indicate? What would local tenderness and warmth over a reducible mass indicate?

A

Incarceration

Strangulation

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71
Q

How do you assess for an inguinal hernia?

A

Occlude deep ring and ask patient to cough (midway between ASIS and pubic symphysis)

Indirect - hernia not restrained (protrudes obliquely behind the scrotum when patient stands)

Direct - hernia restrained (protrudes directly forwards when patient stands)

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72
Q

Differentials for a groin lump?

A

Femoral hernia, hydrodcele, spermatocele, varicocele, undescended testes, lipoma

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73
Q

Repair or an inguinal hernia?

A

Should always be repaired unless specific contraindications

Herniorrhaphy - open (mesh) is preferred

Avoid heavy lifting/straining for a week after

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74
Q

Femoral vs inguinal hernia location?

A 
Inguinal = above and medial
Femoral = below and lateral

TO PUBIC TUBERCLE

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75
Q

What does lateral compartment of femoral canal contain?

A

Medial to lateral

Femoral vein + artery (femoral sheath)
Genitofemoral nerve
Femoral nerve

Medial compartment is the femoral ring, where hernias occur

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76
Q

Who are femoral hernias more common in? What is the aetiology?

A

More common in women - but less common overall than inguinal hernias

Increased intra-abdo pressure - pregnancy, chronic cough, GI obstruction, straining

Laxity or weakness of tissue - pregnancy, rapid weight loss, previous hernia repair

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77
Q

Is incarceration and strangulation more common in femoral or inguinal hernias?

A

Femoral - because it is a smaller hole

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78
Q

How does congenital umbilical hernia occur? Who does it occur in?

A

Occurs through weak umbilical scar

Black children - males 2x more than females

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79
Q

How do acquired para-umbilical hernias occur? Who do they occur in?

A

Just above the umbilicus, weakness of linea alba

5x more common in women than men (age 35-50)

RFs = multiple pregnancy, ascites, obesity, large abdominal tumours

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80
Q

Symptoms and signs of acquired para-umbilical hernia?

A

Sharp pain on coughing/straining

GI symptoms due to traction on stomach/transverse colon

Transient colic due to subacute obstruction

Soon becomes irreducible due to adhesions within the sac

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81
Q

Management of congenital and acquired umbilical hernia?

A

CONGENITAL
Non-intervention successful in 93% of cases. No surgery before age 2.

ACQUIRED
Should be repaired to avoid complications

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82
Q

Who gets gallstones

A

Fat, female, forties, flatulent

90% remain asymptomatic

RFs for becoming symptomatic = smoking/parity

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83
Q

In what situations do gallstones become symptomatic?

A 
Acute cholecystitis
Chronic cholecystitis
Biliary colic
Pancreatitis
Cholangitis
Obstructive jaundice
Gallstone ileus
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84
Q

Management of symptomatic gallstones?

A

NON-SURGICAL
Analgesia (opioids + NSAIDs), adequate hydration, abx

SURGICAL
Cholecystectomy (within 1 week if acute)

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85
Q

What is cholecystitis precipitated by?

Risk factors?

A

Fatty food

Gallstones, female gender, age, obesity, rapid weight loss, pregnancy, Crohn’s disease, hyperlipidaemia

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86
Q

What is Murphy’s sign?

A

pain and cessation of deep inspiration during palpation in RUQ, not present in LUQ

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87
Q

What is Charcot’s triad?

A

fever, RUQ pain, jaundice

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88
Q

Bloods in cholecystitis? Imaging?

Other differentials?

A

↑WCC, ↑CRP, abnormal LFTs
USS – gallstones and thickened, shrunken gallbladder; pericholecystic fluid

Biliary colic – RUQ pain, but no fever/WCC and no jaundice
Cholangitis – RUQ pain and fever/WCC and jaundice

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89
Q

Management of acute cholecystitis?

A

NBM

IV access and bloods
o	FBC (WBC), U&amp;E, glucose, amylase, LFTs

IV analgesia and antiemetic

IV Abx (co-amoxiclav)

Surgery
o Urgent laparoscopic cholecystectomy vs interval procedure. ERCP if distal CBD stone.
o Open procedure required if perforation

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90
Q

How is the portal vein formed?

A

Union of the splenic and the superior mesenteric veins at the level of L2 behind the head of the pancreas

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91
Q

What happens in portal hypertension?

A

blood is diverted into collaterals between the portal and the systemic venous systems

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92
Q

Causes of portal hypertension? (increased resistance)

A

Most common is cirrhosis (worldwide is schistosomiasis)

PRE-HEPATIC
Portal vein thrombosis, splenic vein thrombosis, congenital atresia/stenosis, extrinsic compression

HEPATIC
Pre-sinusoidal = Hepatitis, congenital hepatic fibrosis, idiopathic non-cirrhotic portal hypertension, schistosomiasis
Sinusoidal = cirrhosis

POST-SINUSOIDAL
Budd-Chiari syndrome (hepatic vein thrombosis), veno-occlusive disease, constrictive pericarditis, RHF

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93
Q

Symptoms of portal hypertension?

A

Often asymptomatic with splenomegaly the only sign

Haematemesis of melena – rupture of varices

Hepatic encephalopathy

94
Q

Signs of portal hypertension?

A

Ascites – with low albumin

Porto-systemic shunts – caput medusa

Venous hum

Haemorrhoids

Peripheral oedema

95
Q

Management of portal hypertension (prophylaxis against bleeding)?

A

Conservative = salt restricted diet

Medical = Beta blockers /spiro/furosemide - decreases portal pressure

Surgical = porto-systemic shunt (TIPS procedure) portal vein to hepatic vein

96
Q

What is a TIPS procedure? What is a risk?

A

Transjugular intrahepatic portosystemic shunt

Can cause encephalopathy

97
Q

How are hepatitis A B and C transmitted?

A

A = faecal oral

B = parenteral (blood, body fluids)

C = parenteral (IV drugs, sexual, needlesticks, perinatal)

98
Q

Symptoms of viral hepatitis?

A

N+V, myalgia, fatigue/malaise, RUQ pain, change in sense of smell/taste, coryza, photophobia, headache.

99
Q

Signs of viral hepatitis?

A

Often no signs unless jaundice develops.

Hepatomegaly, splenomegaly and lymphadenopathy may then be present.

100
Q

Complications of viral hepatitis?

A

CHRONIC INFECTION

Consequence of hep B, C or D infection. Presentation varied and may be asymptomatic.

Subclinical infection –> vague symptoms (fatigue/dyspepsia).

Chronic infection –> chronic hepatitis, cirrhosis and hepatocellular carcinoma.

101
Q

Investigations in viral hepatitis?

A

Bloods – FBC, U+E, LFTs, clotting

Hepatitis serology

Imaging – USS/CT/MRI to assess for presence of cirrhosis or other causes of symptoms

102
Q

What is HBsAg?

A

Hep B Surface Antigen

Protein on surface of HBV (patient has infection –> used to make vaccine)

sAgGy face because currently infected

103
Q

What is anti-HBc?

A

Total Hep B Core antibody

Appears at onset of symptoms and persists for life (previous or ongoing infection)

c = CAUGHT IT

104
Q

What is anti-HBs?

A

Hep B surface antibody

Indicates recovery/immunity from hep B

S = SAFE

105
Q

What is IgM anti-HBc?

A

IgM Antibody to Hep B Core Antigen

Acute (<6 months) infection

IgM = OMG acutely infected

106
Q

Management of hep A and B?

A

Avoid unprotected sex.

Treatment mainly supportive (fluids, antiemetics, rest).

Avoid alcohol until liver enzymes normal. Review medications, stop non-essentials.

Treatment with antiviral agents not usually indicated

107
Q

Management of hepatiits C?

A

Aim = prevent cirrhosis, liver failure and cancer developing –> refer to specialist

Early treatment with interferon alpha can reduce chronic infection

Abstinence from alcohol

Barrier contraception

Should not donate blood, organs, tissues or semen

108
Q

What is cirrhosis?

A

Fibrosis and conversion of liver into structurally abnormal nodules –> abnormal vascular relationships

  1. entire liver affected (not focal scarring)
  2. parenchymal injury and fibrosis precedes nodule formation
  3. is irreversible
109
Q

Micronodular and macronodular cirrhosis?

A

Micronodular = <3mm in diameter - alcoholism, wilson’s disease, A-1-antitrypsin deficiency

Macronodular = >3mm in diameter - viral or autoimmune forms of chronic active hepatitis

110
Q

Causes of cirrhosis?

A 
Alcoholic liver disease
Viral hepatitis
Biliary cirrhosis
Haemochromatosis
Wilson's disease
A-1-antitrypsin deficiency
Hepatic venous outflow obstruction (Budd-Chiari syndrome)
111
Q

Signs of cirrhosis?

A

Skin = Jaundice, bruising, spider naevi, skin telangectasias, dupuytren’s contracture

Hands = finger clubbing, leuconychia, palmar erythema

Sexual = gynaecomastia/reduced body hair, erratic menstruation/breast atrophy

Organomegaly = small liver, splenomegaly

112
Q

Symptoms of cirrhosis?

A

Lethargy, itching, fever, weight gain, swelling of abdomen and ankles

113
Q

Complications of cirrhosis?

A

Anaemia (folate deficiency, haemolysis)

Thrombocytopenia (hypersplenism)

Coagulopathy (synthetic function of liver affected, and cholestasis –> reduced vit K absorption)

Varices

Ascites (transudate)

SBP (E.coli)

Hepatocellular carcinoma (Hep C)

114
Q

How does cirrhosis cause ascites?

A

Portal hypertension –> increased capillary pressure –> lymph formation –> ascites

Portal HTN –> splanchnic vasodilation –> RAAS activation and ADH release –> increased retention –> ascites

115
Q

Bloods in cirrhosis?

A

LFTs - AST/ALT raised, gamma-GT raised in active alcoholics

FBC - anaemia, thrombocytopenia, macrocytosis (if alcohol)

U+E - hyponotraemia, renal dysunfction

Albumin - hypoalbuminaemia

Coagulation - PT and INR raised

116
Q

Classification for liver disease?

A

Child Pugh Score

Score >7 –> transplant list

117
Q

Management of cirrhosis?

A

ALCOHOL/NUTRITION
Abstinence, ensure adequate intake, zinc supplementation

PRURITIS
Antihistamines/topical ammonium lactate
Colestyramine is mainstay

PREVENTING COMPLICATIONS
Osteoporosis prevention, regular exercise to prevent wasting
Prophylactic Abx
Vaccination - hep A, influenza, pneumococcal
Avoid hepatic metabolised drugs
Surveillance of varices/cancer

TRANSPLANTATION

118
Q

What can you give in hepatic encephalopathy?

A

High dose lactulose

Avoid CNS depressants, use haloperidol instead

119
Q

Definition of transudate and exudate?

A

Trans = protein <3g per 100ml of fluid
Caused by increased hydrostatic pressure or reduced oncotic pressure

Ex = protein >3g per 100ml of fluid
Caused by inflammation

120
Q

Specific causes of ascites?

A

TRANSUDATE
Cirrhosis, HF, nephrotic syndrome, constrictive pericarditis, ovarian tumours

EXUDATE
Malignant disease, pyogenic infection, TB, pancreatitis, lymphoedema/myxoedema

121
Q

Investigation of choice in ascites?

A

USS + Diagnostic paracentesis

30-50ml of fluid withdrawn to allow identification of…

Protein count (albumin and total protein)
Malignant cells
Bacteria
WBCs (if >250 then SBP)
Glucose
122
Q

Management of ascites?

A

Therapeutic paracentesis of 4-6 litres

Plasma volume expansion with albumin

Bed rest, reduced salt intake, spironolactone

123
Q

Areas affected in UC and Crohn’s?

A

Crohn’s = all GI tube, mainly terminal ileum and ascending colon, rectum in 50% of cases

UC
Rectum always involved
Colon, appendix and terminal ileum may be involved
Pancolitis = involvement beyond splenic flexure

124
Q

Macroscopic appearance in Crohn’s?

A 
Small bowel thickened
Deep ulcers and fissures
Cobblestone appearance
Fistula and abscesses in colon
Apthoid ulceration is early feature
Granulomas present (50-60%)
Non caesating epitheloid cell aggregates with Langhan’s giant cells
125
Q

Macroscopic appearance in UC?

A 
Mucosa is reddened
Inflamed and bleeds easily
Ulcers may be present if severe
Pseudopolyps formed by inflammation
Mainly mucosal
Inflammatory cells in lamina propria
No granulomas
126
Q

Which IBD has strictures?

A

Crohn’s

127
Q

Which IBD has crypt abscesses?

A

UC

128
Q

Which IBD has goblet cell depletion?

A

UC

129
Q

Extra-intestinal features of IBD?

A 
Clubbing
Uveitis
Arthritis
Erythema nodosum
Pyoderma gangenosum (HLA-B27)
130
Q

Complications of Crohn’s

A

SBO
Toxic dilatation
Abscess formation

Fistulae (infalmmation –> stricture –> obstruction –> fistulae) - colovesical, colovaginal ,perianal, enterocutaneous

Perforation
Malnutrition
Rectal haemorrhage

CANCER

131
Q

Complications of UC?

A

Perforation/bleeding
Toxic dilatation of the colon
VTE – prophylaxis for all inpatients
Colonic cancer

132
Q

Bloods in IBD?

A

FBC, ESR, CRP, U+E, LFT, blood culture, (INR, ferritin, B12, folate in Crohn’s due to TI involvement)

133
Q

Stool stuff in IBD?

A

MC+S
Exclude campylobacter, C.dff, Salmonella, Shigella, E.coli, amoebae

Faecal Calprotectin
Recommended to distinguish between IBS/IBD

134
Q

AXR signs in IBD?

A

Thumbprinting = wall oedema = active disease

Lead pipe colon = chronic disease (featureless)

135
Q

Fluoroscopy in IBD?

A

BARIUM ENEMA
Not during acute attack

Crohn’s - cobblestoning and strictures (string sign), ‘rose thorn ulcers’

UC - lead piping

SMALL BOWEL ENEMA
Detects ileal disease in Crohn’s

136
Q

Staging of IBD?

A

Trulove and Wit’s criteria

137
Q

Inducing remission in IBD?

A 
CROHN'S
•	Steroids (oral or IV)
•	Enteral nutrition - in younger people
•	Azathioprine, mecaptapurine, methotrexate
•	Smoking cessation can induce remission

UC
• Oral mesalazine/ sulfasalazine
• Steroids (Oral or IV)

138
Q

Maintenance in IBD?

A

CROHN’S
• Azathioprine, mecaptapurine, methotrexate
• Infliximab, adalimumab – in patients that don’t respond to treatment (mabs = TNF-a inhibitors)

UC
• Oral mesalazine/ sulfasalazine
• Rectal treatments often given – salazine enema
• Immunosuppressants (Azozthiprine, mecaptopurine) can be used
• Cyclopsorin for refractory colitis – large side-effect profile

139
Q

Surgery in IBD?

A

CROHN’S
Indicated in limited disease, refractory disease, life-threatening flares

UC
Can be curative – indicated in disease refractory to medical treatment, life-threatening acute flares, or treatment of complications (carcinoma)

140
Q

Surveillance of IBD patients?

A

Regular scoping for cancer

141
Q

What causes diverticulae?

A

Lack of dietary fibre –> hypertrophy of longitudinal and circular muscle

Increased intraluminal pressure –> outpouching

142
Q

Where are diverticulae most often found?

A

Sigmoid colon

143
Q

Symptoms of diverticulosis?

A

Pain/indigestion - not worsened by food; distension, flatulence, belching

Constipation - infrequent motions and hard stool

Appetite and weight normal

144
Q

Symptoms of acute diverticulitis?

A

Severe LIF pain exacerbated by movement

Abdo distension

Nausea and anorexia

Constipation and diarrhoea

145
Q

Symptoms of chronic diverticulitis?

A

MIMICS COLON CANCER

Diarrhoea alternating w/constipation

Vomiting, distension, colicky abdo pain

Passage of mucus, bright red blood or melena

146
Q

Complications of diverticular disease?

A 
Obstruction due to stricture
Abscess
Perforation
Fistula
Haemorrhage
147
Q

Investigations in diverticular disease?

A

DIAGNOSIS OF EXCLUSION

Barium meal/enema - shows outpouchings of diverticula and narrowed sigmoid colon

Sigmoidoscopy - shows inflammation but poor at showing diverticula

CXR - rule out perforation

148
Q

Management of acute diverticulitis?

A

Bed rest
IV ceph and met/fluids
Analgesia

149
Q

Indications for surgery in diverticulitis?

A 
Peritonitis
Fistula formation
Persistent haemorrhage
Pericolic abscess formation
Intestinal obstruction
Recurrent diverticulitis resistant to medical therapy
150
Q

Management of chronic diverticular disease?

A

High fibre diet
Antispasmodics
Laxatives (lactulose)

151
Q

Where is McBurney’s point?

A

1/3 distance from ASIS to umbilicus

152
Q

What is Psoas sign?

A

Pain on extending hip if retrocaecal appendix

153
Q

PR in appendicitis?

A

Tender on the right (sign of low-lying appendix)

154
Q

Investigations in appendicitis?

A 
BLOODS
FBC, U+E, LFT, CRP, G+S (WCC raised, neutrophilia, raised CRP)
Blood cultures (if pyrexial)

Urine PT and urinalysis

USS and CECT (if appropriate)

155
Q

Immediate management of appendicitis?

A

NBM
IV fluids
Analgesia
IV abx pre-op (ceph and met or co-amoxiclav)

Appendicectomy

156
Q

Causes of bowel obstruction?

A 
SMALL = adhesions and hernias
LARGE = tumours and volvulus

Others = intussception, IBD, gallstone ileus, foreign bodies

157
Q

AXR signs in bowel obstruction?

A

Excess gas in abnormall dilated bowel loops

Bowel proximal to obstruction dilates

Bowel distal to obstruction shrinks and collapses

158
Q

Management of bowel obstruction?

A

DRIP AND SUCK

NBM and IV fluids
NGT in SBO or if vomiting - minimises risk of aspiration
Pain relief
IV abx

Conservative treatment for 2-3 days (unless causes by an incarcerated hernia)
If no resolution, or deterioration –> surgery

159
Q

Causes of ileus?

A

ABDOMINAL - post-op, peritonitis, vascular occlusion

SYSTEMIC - hypokalaemia, DKA, uraemia, hypoT, hypomagnasaemia

DRUGS - anticholinergics, TCAs, parkinsonian drugs

REFLEX CAUSES - postpartum, renal colic, retroperitoneal haemorrhage

160
Q

Most common sites of gallstone ileus?

A

Ileum (60%)
Jejunum (15%)
Stomach (15%)
Colon (5%)

161
Q

Most common places for colorectal cancer?

A

Rectum (27%)
Caecum and ascending (22%)
Sigmoid (20%)

162
Q

Features of right-sided colon cancer?

A

Weight loss, anaemia, painful palpable RIF mass, rectal bleeding

More likely to be advanced at presentation

163
Q

Features of left-sided colon cancer?

A

Early change in bowel habit, colicky pain, rectal bleeding, bowel obstruction, tenesmus, mass in LIF

Less advanced at presentation

164
Q

Features of rectal colon cancer?

A

Change in bowel habit commonest feature, bleeding, rarely associated with pain

165
Q

Investigations in colon cancer?

A

BLOODS - FBC, LFT

Colonoscopy = gold standard

Barium enema/flexible sigmoidoscopy = patient with major co-morbidity. APPLE CORE SIGN

CT colonograpy = substantially less invasive and does not require sedation

166
Q

Who is offered colon cancer screening?

A

Age 60-69 (being extended to 74)

Every 2 years

FOB test - if abnormal –> colonoscopy

And high risk individuals - age >40, fhx of colon ca, personal hx of colon ca, FAP, UC

167
Q

Rome criteria for IBS?

A

Abdo pain (or discomfort) - relieved by defecation or associated with altered stool form or frequency

More than 2 of...
Urgency
Incomplete evacuation
Abdominal bloating/distension
Mucous PR
Worsening of symptoms after food
168
Q

Investigations in IBS-type picture?

A

Bloods - FBC, U+E, CRP, LFT, coeliac serology

Colonoscopy - if features of systemic disease

Serum CA-125 - exclude ovarian cancer

169
Q

Symptomatic treatment in IBS?

A

Constipation –> laxatives
Diarrhoea –> loperamide after each loose stool
Colic/bloating –> buscopan

170
Q

Causes of rectal prolaspe?

A

Pelvic floor muscle weakness, prior pelvic surgery

Neurologic disorders = CVA, dementia, pudendal neuropathy

Other = multiparity

171
Q

Symptoms of rectal prolapse?

A

Something coming down - during defecation, mucous and bleeding

Dull anal pain - indicates strangulation (constitutional symptoms - fever, chills, sweating, N+V)

Faecal incontinence - passive (leakage they are unaware of) urge (unable to get to toilet in time)

Majority also have urinary incontinence

172
Q

Rectal prolapse on examination?

A

Protruding mass with concentric rings of mucosa

Differentiate mucosal prolapse (thin, segmental) from full thickness (circumfrential, plum coloured, with mucosal folds)

173
Q

Management of rectal prolapse?

A

Conservative - manual reduction, circumanal ring

Surgical - abdominal procedures preferred if patient fit as perineal procedures have higher rate of recurrence

174
Q

What are haemorrhoids? Where do they arise?

A

Abnormally enlarged vascular muscosal cushions in the anal canal

Above the dentate line = internal
Below the dentate line = external

Dentate line = 2cm above the anal verge (anatomical delineation between upper and lower canal)

175
Q

Grading of haemorrhoids?

A

Grade 1 = do not prolapse out of canal
Grade 2 = prolapse of defecation but reduce spontaneously
Grade 3 = require manual reduction
Grade 4 = cannot be reduced

176
Q

Who do haemorrhoids affect more?

A

Men, and affects them for longer

Women affected at certain periods - pregnancy and perperium

177
Q

Causes of hamorrhoids?

A

Constipation and prolonged straining and stool (low fibre diet)

Increased anal sphincter tone

Obstruction of venous flow (pregnancy, portal hypertension)

178
Q

Symptoms of haemorrhoids?

A

Bright red painless bleeding after defecation

Faecal soiling

Mucus discharge

Pruritis ani

Rectal fullness, discomfort or incomplete evacuation

Prolapsed –> lump at anal verge

179
Q

Examination of haemorrhoids?

A

EXTERNAL

  • Not visible if not prolapsed
  • Local perineal irritation
  • Straining may make them visible at anal verge
  • Thrombosed haemorrhoids are purple, swollen and acutely tender perianal lumps

RECTAL

  • internal haemorrhoids not palpable (they empty with finger pressure)
  • Excludes other pathology (cancer)
180
Q

Complications of haemorrhoids?

A

Strangulation

181
Q

Investigations for haemorrhoids?

A

Proctoscopy – to diagnose first or second degree piles (seen bulging into lumen as proctoscope is withdrawn)

Sigmoidoscopy – indicated if history of bleeding or symptoms suspicious of malignancy

182
Q

Conservative management of hamorrhoids?

A

Ensuring perineum is dried and washed after defaecation (prevents pruritis ani) – application of talcum powder

Digital replacement of prolapsed haemorrhoids

Local anaesthetic creams and ointments

Treatment aimed at reducing spasm of internal anal sphincter (Nitroglycerine ointments, Botulinum toxin injection)

183
Q

Surgical management of harmorrhoids?

A

Sclerotherapy, rubber band ligation, cryotherapy (small piles)

Anal dilatation under GA, haemorrhoidectomy (big piles)

184
Q

Prevention of haemorrhoids?

A

Eat more fibre and bulk up stools

Minimise time spent defecating

185
Q

How does perianal abscess arise?

A

Infection in perianal gland (lies between internal and external sphincters)

Glands are V small and become obstructed by faeces –> infection

186
Q

Conditions that pre-dispose to perianal abscess?

A

TB, actinomycosis, mucinous carcinoma, IBD (esp Crohn’s)

Men affected more than women

187
Q

Symptoms of perianal asbcess?

A

Gradual onset pain around the anus

Becomes more severe and throbs. Defaecation and sitting are painful.

Sitting with one buttock raised is pathognomonic

188
Q

Signs of perianal asbcess?

A

Abscess may be seen deep in the skin next to the anus.

Localised tenderness and swelling.

Proctoscopic examination –> may see damaged opening to affected gland, with pus discharging from it.

189
Q

Investigations for perianal abscess?

A

None usually necessary – rectal exam usually sufficient for diagnosis.

Screen for STDs/investigate for IBD, diverticular disease or lower GI malignancy.

Culture pus for routine gut and skin organisms

190
Q

Management of perianal abscess?

A

Surgical drainage if established

Medication for pain relief

Abx not usually necessary unless diabetes or immunocompromised (if found early, abx may abort the infection).

191
Q

Complications of I+D for perianal abscess?

A

31% of I+D patients develop fistula

192
Q

Where do anal fissures usually arise?

A

Directly posteriorly and in the midline

Longitudinal tears

193
Q

Who do anal fissures affect?

A

Men and women equal

20-30 years peak

Secondary to IBD (Crohn’s)

194
Q

What is a sentinel pile?

A

Torn, bunched up strip of mucosa at the base of a fissure

195
Q

Consevative/medical management of anal fissures?

A

Warm baths, stool softeners, bulk laxatives, add bran to diet, analgesia, reassurance

Topical GTN/diltiazem

Botulinum toxin (if topical GTN fails)

196
Q

Surgical management of anal fissure?

A

Internal sphincterotomy

Manual diltation (reduces sphincter pressure - rarely indicated as can cause incontinence)

197
Q

Cause of sigmoid volvulus?

A

Chronic constipation –> baggy, atonic bowel

May become twisted on mesenteric axis and produce a closed loop obstruction

Venous infarction –> perforation and faecal peritonitis

198
Q

Who gets sigmoid volvulus?

A

Elderly constipated patients

M:F 4:1

More common than caecal (younger)

199
Q

Feature of history in sigmoid volvulus other than obstruction things?

A

Previous episodes - colonic twists may spontaneously untwist

200
Q

Feature of rectal exam in sigmoid volvulus?

A

Capacious, empty rectum

201
Q

Features of AXR in sigmoid volvulus?

A

Enormously dilated oval gas shadow in upper abdomen (gas-filled hepatic flexure)

May be looped on itself to give inverted U “coffee bean sign”

202
Q

Management of sigmoid volvulus?

A

Decompression with flatus tube

Laparoscopic derotation or laparotomy +/- bowel resection

203
Q

Prevention of recurrence of sigmoid volvulus?

A

Sigmoidplexy

204
Q

What is achalasia?

A

Neuromuscular failure of relaxation at the distal oesophagus

Progressive dilatation, tortuosity, incoordination of peristalsis and often hypertrophy of the oesophagus above.

A functional obstruction

205
Q

When and how does achalasia present?

A

Any age (peak 30-40, both sexes equal)

Dysphagia (progressive, less rapid than cancer, more for solids than liquids)

Regurgitation –> vomiting or aspiration

Chronic malnourishment

206
Q

Management of achaliasa?

A

Surgical management

Botulinum toxin

Nitrates/CCBs (least effective)

207
Q

Causes of chronic pancreatitis?

A 
Alcohol (by far biggest cause)
Familial
CF
Haemochromatosis
Pancreatic duct obstruction
↑PTH
Congenital (pancreas divisum
208
Q

Features of chronic pancreatitis?

A 
epigastric pain
Anorexia and weight loss
Exocrine insufficiency
Endocrine insufficiency
Obstructive jaundice
Portal hypertension
Pancreatic duct strictures
209
Q

Exocrine and endocrine insufficiency in chronic pancreatitis?

A

EXOCRINE
o Steatorrhoea
o Hypocalcaemia (unabsorbed fat chelates calcium)
o Malabsorption of fat (but no bleeding tendency)
o Protein catabolism (exacerbates weight loss)

ENDOCRINE
Impaired glucose tolerance

210
Q

Biochemical profile of chronic hepatitis?

A

Raised aminotransferases out of proportion of alk phos

Conjugated hyperbilirubinaemia

Prolongation of PT which is resistant to correction with parenteral vitamin K

211
Q

What is a subphrenic abscess?

A

Localised collection of pus underneath right/left hemidiaphragm.

Usually the result of a breach in integrity of the peritoneum.

Occur as result of generalised peritonitis (appendicitis, perforated ulcer, perforated gallbladder, faecal contamination).

212
Q

Clinical picture of a subphrenic abscess?

A

Patient who develops features of toxicity 2-21 days after making initial recovery from an episode of peritonitis or an operation

Swinging fever
Malaise, nausea, weight loss
Upper abdo pain radiating to shoulder tip
Breathlessness (lower lung collapse or development of pleural effusion)

213
Q

How is subphrenic abscess diagnosed?

A

Diagnosed using USS or abdominal CT

CXR: high diaphragm on affected side, gas and fluid below diaphragm, may be pleural effusion

214
Q

Features of liver abscess?

A

Fever, RUQ pain, tender hepatomegaly.

Rarely jaundice and referred shoulder tip pain. •

Raised alk phos/gamma GT
Normal/moderately increased serum bilirubin
Due to enzyme induction in parts of liver where there is impaired bile excretion

215
Q

Causes of liver abscess?

A

Bacterial - usually polymicrobial (strep milleri)

Amoebic - entamoeba hystolitica

Fungal - candida

216
Q

Risk factors for hepatocellular carcinoma?

A

Liver cirrhosis (80% cases – any cause)

Chronic HBV/HCV carriage

Drugs (anabolic steroids, COCP)

Toxins (aflatoxin)

Parasites (schistosomiasis, echinococcus, clonorchis sinensis)

217
Q

Features of hepatocellular carcinoma?

A

General = malaise, fever

GI = anorexia, jaundice, constipation, ill-defined upper abdominal pain, abdominal fullness, bleeding oesophageal varices

Hepatomegaly = liver is often irregular or nodular, may be tender

Ascites

Dyspnoea

218
Q

Spread of hepatocellular ca?

A

lung, bone, brain, lymph nodes (right supraclavicular)

219
Q

Classification of acute hepatic failure?

A

Severe hepatic dysfunction within 6 months of onset of symptoms –> encephalopathy or coagulopathy

Hyperacute = within 7 days
Acute = within 8-28 days
Subacute = within 5-12 weeks
220
Q

What is chronic (decompensated) liver disease?

A

Deterioration in liver function superimposed on chronic liver disease

221
Q

Presentation of hepatic failure?

A

CNS - encephalopathy

Renal failure

Sepsis - bacterial infection w/o fever and leucocytosis

Coagulpathy

CVS - HF and hypotension if heart disease

Metabolic - hypoglycaemia

Hypoxia

222
Q

Why is there coagulopathy in liver failure?

A

Synthesis of coagulation factors (I, II, V, VII, IX, X) affected.

Inhibition of fibrinolysis (liver produces protein C, protein S and antithrombin III)

Clearance of activated coagulation factors affected (liver removes fibrin and tPA from circulation)

Absorption of vitamin K affected (malabsorption)

223
Q

Why is there encephalopathy in liver failure?

A

Accumulation of toxins from gut –> cerebral oedema and changes in level of consciousness –> coma.

224
Q

What causes an epigastric hernia? Who gets them?

A

Protrusion of extra-peritoneal fat where linea alba is pierced by a blood vessel

Drags a pouch of peritoneum with it

Age 20-50 and more women than men

225
Q

Symptoms of epigastric hernia?

A

Pain - aggravated by eating

Abdominal mass
Vomiting/nausea
Relieved by reclining

226
Q

3 polyposis coli syndromes?

A

FAP
Gardner’s syndrome
Turcot’s syndrome

All autosomal dominant and require endoscopic surveillance from teenage years

227
Q

What are Gardner’s and Turcot’s also associated with?

A

Gardner’s - soft tissue and bone tumours

Turcot’s - malignant CNS tumours

228
Q

Anal carcinoma types?

A

Most = squamous

Other = bcc/melanoma of overlying skin

229
Q

Presentation of anal carcinoma?

A

Mainly occurs in elderly

Anal pain and discomfort

Discharge and bleeding (similar to haemorrhoids)

Enlarged groin LNs indicate metastasis

O/E – may feel hard and woody due to invasion of perianal tissues

230
Q

Presentation of perianal haematoma?

A

Caused by rupture of a blood vessel beneath the anal skin – acutely painful and onset after straining at stool.

O/E - blue-black bulge in the skin near the margin of the anus

231
Q

What is fistula-in-ano? Causes?

A

Abnormal communication between the perianal skin and the anal or rectal lumen (both epithelial surfaces)

Chronic version of peianal abscess

Causes = Crohn’s, TB, HIV, previous surgery, radiotherapy, trauma, foreign bodies, anorectal cancer

232
Q

Presentation of fistula-in-ano?

A
  • Intermittent discharge in perianal region
  • Pain and discomfort in perianal area
  • Chronic irritation

External opening of fissure generally seen lateral to anus – may be seen as a small papilla of granulation tissue.
Internal opening may be felt on rectal examination.

- FINALS (24 decks)

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