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1
Q

Causes of bloody diarrhoea

A 
 ischaemic colitis
 campylobacter, shigella, salmonella, E. coli,
amoeba, pseudomembranous colitis
 UC, Crohn’s
 CRC, polyps
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2
Q

Causes of pus in stools

A

IBD, diverticulitis, abscess

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3
Q

Management for diarrhoea

A

Treat cause

Oral or IV rehydration

Codeine phosphate or loperamide after each loose stool

Anti-emetic if assoc. n/v: e.g. prochlorperazine

Abx (e.g. cipro) in infective diarrhoea → systemic illness

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4
Q

What is C.diff

A

 Gm+ve spore-forming anaerobe
 Release enterotoxins A and B
 Spores are v. robust and can survive for >40d

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5
Q

Risk factors for c.diff infection

A

 Abx: clindamycin, cefs, co-amox, ciprofloxacin
- up to 2m after
 ↑age
 In hospital: ↑ ̄c length of stay, ↑ ̄c C. diff +ve contact
 PPIs

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6
Q

Clinical presentation of infection with c.diff

A 
 Asymptomatic
 Mild diarrhoea
 Colitis 
 Pseudomembranous colitis
- fever, dehydration, abdo pain, bloody diarrhoea, mucus PR
 Fulminant colitis
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7
Q

Investigations for c.diff

A

 Bloods: ↑↑CRP, ↑↑WCC, ↓albumin, dehydration
 CDT ELISA -toxin A&B
 Stool culture

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8
Q

Complications of c.diff infection

A

 Paralytic ileus
 Toxic dilatation → perforation
 Multi-organ failure

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9
Q

Management of c.diff

A

Barrier nursing - put in side room
 Stop causative Abx
 Avoid antidiarrhoeals and opiates
 Enteric precautions

1st line: Metronidazole 2wk 2nd line: Vanc 125mg
Severe: Vanc 1st

Urgent colectomy may be needed if
 Toxic megacolon
 ↑ LDH
 Deteriorating condition

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10
Q

Causes of constipation

A 
OPENED IT
Obstruction - mechanical (adhesion/hernia/ca) or post op ileus
Pain - fissure
Endocrine/ electrolytes - ↓T4, ↓Ca, ↓K, uraemia
Neuro - MS, Myelopathy, Cauda Equina
Elderly
Diet/ Dehydration
IBS
Toxins - opiods
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11
Q

Management of constipation

A

 Drink more
 ↑ dietary fibre

Bulking: ↑ faecal mass → ↑ peristalsis - fybogel (Ispaghula husk)
 CI: obstruction and faecal impaction

Osmotic: retain fluid in the bowel - Lactulose

Stimulant: ↑ intestinal motility and secretion - Senna
 CI: obstruction, acute colitis
 SE: abdo cramps

Softeners
 For painful anal condition - Liquid paraffin

Phosphate enema (osmotic)

Suppositories
 Glycerol (stimulant)

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12
Q

Diagnosis of IBS

A

Abdo discomfort / pain for ≥ 12wks which has 2 of:
 Relieved by defecation
 Change in stool frequency (D or C)
 Change in stool form: pellets, mucus

 \+2of:
 Urgency
 Incomplete evacuation
 Abdo bloating / distension
 Mucous PR
 Worsening symptoms after food
Exclusion criteria 
 >40yrs
 Bloody stool
 Anorexia
 Wt. loss
 Diarrhoea at night
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13
Q

Management of IBS

A

Bloods - incl Coeliac and TSH
+/- colonoscopy

  • Exclusion diets can be tried
  • Fybogel for constipation and diarrhoea
  • Antispasmodics for colic/bloating (e.g. mebeverine)
  • Amitriptyline may be helpful
  • CBT
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14
Q

Causes of dysphagia

A 
Inflammatory
 Tonsillitis, pharyngitis
 Oesophagitis: GORD, candida
 Oral candidiasis
 Aphthous ulcers

Mechanical Block 
-  Luminal
 FB
 Large food bolus 
- Mural
> Benign stricture
 Web (e.g. Plummer-Vinson)
 Oesophagitis
 Trauma (e.g. OGD)
> Malignant stricture-  Pharynx, oesophagus, gastric
 Pharyngeal pouch
- Extra-mural
 Lung Ca
 Rolling hiatus hernia
 Mediastinal LNs (e.g. lymphoma) 
 Retrosternal goitre
 Thoracic aortic aneurysm

Motility Disorders 
- Local
Achalasia
 Diffuse oesophageal spasm
 Nutcracker oesophagus
 Bulbar / pseudobulbar palsy (CVA, MND)
- Systemic
 Systemic sclerosis / CREST 
 MG
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15
Q

Presentation of dysphagia

A

 Dysphagia for liquids and solids at start
- Yes: motility disorder
- No, solids > liquids: stricture
 Difficulty making swallowing movement: bulbar palsy
 Odonophagia: Ca, oesophageal ulcer, spasm
 Intermittent: oesophageal spasm
 Constant and worsening: malignant stricture
 Neck bulges or gurgles on drinking: pharyngeal pouch

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16
Q

Signs that dysphagia could present with

A 
 Cachexia
 Anaemia
 Virchow’s node (+ve = Troisier’s sign)
 Neurology
 Signs of systemic disease (e.g. scleroderma)
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17
Q

Investigations for dysphagia

A

URGENT upper GI endoscopy +- biopsy (if >55, with weight loss, abdo pain, dyspepsia)

 Bloods: FBC, U+E
 Barium swallow ± video fluoroscopy
 Oesophageal manometrry
 +- USS/EUS/CT thorax

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18
Q

Pathophysiology of achalasia

A

 Degeneration of myenteric plexus (Auerbach’s)
 ↓ peristalsis
 LOS fails to relax
- most commonly idiopathic

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19
Q

Presentation of achalasia

A

 Dysphagia: liquids and solids at same time
 Regurgitation
 Substernal cramps
 Wt. loss

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20
Q

Investigations for achalasia

A

 Ba swallow: dilated tapering oesophagus (Bird’s beak)
 Manometry: failure of relaxation + ↓ peristalsis
 CXR: may show widended mediastinum
 OGD: exclude malignancy

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21
Q

Rx of achalasia

A

 Med: CCBs, nitrates
 Int: endoscopic balloon dilatation, botulinum toxin injection
 Surg: Heller’s cardiomyotomy (open or endo)

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22
Q

Pharyngeal pouch pathophysiology

A

Outpouching of oesophagus between upper boarder of cricopharyngeus muscle and lower boarder of inferior constrictor of pharynx
 Weak area called Killian’s dehiscence.
 Defect usually occurs posteriorly but swelling usually bulges to left side of neck.
 Food debris → pouch expansion → oesophageal
compression → dysphagia.

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23
Q

Presentation and rx of a pharyngeal pouch

A

Pres: regurgitation, halitosis, gurgling sounds

Rx: excision, endoscopic stapling

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24
Q

Diffuse oesophageal spasm presentation

A

 Intermittent chest pain ± dysphagia

 Ba swallow shows corkscrew oesophagus

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25
Nutcracker oesophagus presentation
 Intermittent dysphagia ± chest pain | ↑ contraction pressure ̄c normal peristalsis
26
Causes of an oesophageal rupture
- Iatrogenic - endoscopy, biopsy, dilatation - violent emesis (boerhaave's syndreom) - carcinoma - Trauma (surgical emphysema ±pneumothorax)
27
Features of oesophageal rupture
- Odonophagia - Mediastinitis (tachypnoea, dyspnoea, fever, shock) - surgical emphysema
28
management of oesophageal rupture
PPI, Abx, NGT
29
Symptoms of dyspepsia
```  Epigastric pain  Bloating  Heartburn ALARM  Anaemia  Loss of wt.  Anorexia  Recent onset progressive symptoms  Melaena or haematemesis  Swallowing difficulty ```
30
Causes of dyspepsia
 Inflammation: GORD, gastritis, PUD  Ca: oesophageal, gastric  Functional: non-ulcer dyspepsia
31
Management of new onset dyspepsia
``` OGD if >55 or ALARMS - Try conservative for 4 weeks > stop NSAIDS, CCBS > Lose wt., stop smoking, ↓ EtOH > Avoid hot drinks and spicy food > OTC - Antacids/gaviscon ``` - Test for H. pylori if no improvement: breath or serology  +ve → eradication therapy  -ve → PPI trial for 4wks OGD if no improvement
32
Eradication therapy for H.Pylori
Triple therapy for 1 week - PPI - Amoxicillin - Clarithromycin
33
Presentation of Duodenal Ulcers v gastric ulcers
``` DU Epigastric pain:  Before meals and at night  Relieved by eating or milk GU  Epigastric pain:  Worse on eating  Relieved by antacids  Wt. loss ```
34
Risk factors for PUD
``` H. pylori (90%)  Drugs: NSAIDs, steroids  Smoking  EtOH  gastric emptying (↑ DU, ↓GU)  Blood group O (PU)  Stress --> Cushings, burns, sepsis, trauma ```
35
Complications of PUD
Haemorrhage  Haematemeis or melaena  Fe deficiency anaemia Perforation  Peritonitis and distension, vomiting Gastric Outflow Obstruction  Vomiting, colic, distension, succission splash Malignancy  ↑ risk ̄c H. pylori
36
Investigations for PUD
 Bloods: FBC, urea (↑ in haemorrhage)  C13 breath test  OGD (stop PPIs >2wks before)  Campylobacter-like organism test (CLO) / urease test for H. pylori (urea --> CO2 + ammonia - neutralises stomach acid)  Biopsy ulcer to check for Ca  Gastrin levels if Zollinger-Ellison suspected
37
Conservative Management of PUD
```  Lose wt.  Stop smoking and ↓ EtOH  Avoid hot drinks and spicy food  Stop drugs: NSAIDs, steroids  OTC antacids ```
38
Medical management of PUD
```  OTC antacids: Gaviscon, Mg trisilicate  H. pylori eradication  Full-dose acid suppression for 1-2mo  PPIs: lansoprazole 30mg OD  H2RAs: ranitidine 300mg nocte  Low-dose acid suppression PRN ```
39
Surgical management of PUD
 No acid → no ulcer  Acid secretion stimulated by gastrin and vagus N. Vagotomy +/- antrectomy ( distal half of stomach removed) Subtotal gastrectomy
40
Complications of gastric surgery
``` Physical  Stump leakage  Abdominal fullness  Reflux or bilious vomiting (improves ̄c time)  Stricture ``` Metabolic - Dumping syndrome  Abdo distension, flushing, n/v Early: osmotic hypovolaemia  Late: reactive hypoglycaemia - Blind loop syndrome → malabsorption, diarrhoea  Overgrowth of bacteria in duodenal stump  Anaemia: Fe + B12  Osteoporosis - Wt. loss: malabsorption of ↓ calories intake
41
Pathophysiology of GORD
LOS dysfunction → reflux of gastric contents → oesophagitis.
42
Risk factors for GORD
```  Hiatus hernia  Smoking  EtOH  Obesity  Pregnancy  Drugs: anti-AChM, nitrates, CCB, TCAs  Iatrogenic: Heller’s myotomy ```
43
Symptoms of GORD
``` Oesophageal  Heartburn  Related to meals  Worse lying down / stooping  Relieved by antacids  Belching  Acid brash, water brash  Odonophagia  Hoarseness ``` Extra-oesophageal  Nocturnal asthma  Chronic cough  Laryngitis, sinusitis
44
Anti- reflux mechanisms
- LOS - Angle of His - Pressure in abdominal cavity higher than thoracic - R crus of diaphragm acts as a sling around oesophagus
45
Complications of GORD
 Oesophagitis: heartburn  Ulceration: rarely → haematemesis, melaena, ↓Fe  Benign stricture: dysphagia  Barrett’s oesophagus - metaplasia of squamous to gastric columnar epithelium and goblet cell  Oesophageal adenocarcinoma - Metaplasia → dysplasia → adenocarcinoma
46
Differential diagnosis of GO reflux
``` Oesophagitis  Infection: CMV, candida  IBD  Caustic substances / burns PUD Oesophageal Ca ```
47
Investigations for GORD
``` Isolated - no Ix Bloods: FBC CXR: hiatus hernia may be seen OGD if:  >55yrs  Symptoms >4wks  Dysphagia  Persistent symptoms despite Rx  Wt. loss  OGD allows grading by Los Angeles (A-D) Classification Ba swallow: hiatus hernia, dysmotility 24h pH testing ± manometry  pH <4 for >4hrs (demeester score) ```
48
Conservative management of GORD
```  Lose wt.  Raise head of bed  Small regular meals ≥ 3h before bed  Stop smoking and ↓ EtOH  Avoid hot drinks and spicy food  Stop drugs: NSAIDs, steroids, CCBs, nitrates ```
49
Medical management of GORD
```  OTC antacids: Gaviscon, Mg trisilicate  1: Full-dose PPI for 1-2mo  Lansoprazole 30mg OD  2: No response → double dose PPI BD  3: No response: add an H2RA  Ranitidine 300mg nocte  Control: low-dose acid suppression PRN ```
50
Surgical management, indications and complications of GORD
``` Nissen Fundoplication - Mobilise gastric fundus and wrap around lower oesophagus - Indications: all 3 of:  Severe symptoms  Refractory to medical therapy  Confirmed reflux (pH monitoring) ``` ``` Complications - Gas-bloat syn.: inability to belch / vomit - Dysphagia if wrap too tight OTHER Radiofrequency ablation. magnetic beads ```
51
Classifications of hiatus hernias
Sliding (80%)  GOJ slides up into chest  assoc.GORD Rolling (15%)  GOJ remains in abdomen but a bulge of stomach rolls into chest alongside the oesophagus  LOS remains intact so GORD uncommon  Can → strangulation Mixed (5%)
52
Gastric volvulus symptoms
Borchardt's triad - severe epigastric pain - retching without vom - inability to pass NG tube
53
Ix for hiatus hernia
OGD: assess for oesophagitis and upwards displacement GOJ CXR: gas bubble and fluid level in chest 24h pH + manometry: exclude dysmotility or achalsia Ba Swallow
54
Rx of hiatus hernias
Lose wt. Rx reflux Surgery if intractable symptoms despite medical Rx OR rolling - funoplication/ curoplasty
55
Risk factors for hiatus hernia
``` Age (reduced diaphragm tone) raised intra-abdo pressure 0 pregnancy 0 obesity 0 ascites ```
56
Differentials of Haematemesis
VINTAGE ``` Varices Inflammation (PUD/ oesopha/gastr- itis) Neoplasia (oesoph/gastric) Trauma (Mallory-weiss/ Boerhavve) Angiodysplasia/ HHT/ Dieulafoy lesion Generalised bleeding diathesis - warfarin, thrombolytics, CRF Epistaxis ```
57
Difference between mallory-weiss and boerhaave's
Mallory-Weiss - mucosal Tear Boerhaave’s Syndrome - Full-thickness tear  2cm proximal to LOS
58
Signs on examination after an Upper GI bleed
```  Signs of CLD - telangectasia, purpura, jaundice  PR:melaena  Shock? - Cool, clammy, CRT>2s - ↓BP (<100) or postural hypotension (>20 drop) - ↓ urine output (<30ml/h) - Tachycardia - ↓GCS - ↓ JVP ```
59
What is the Rockall score
``` Prediction of re-bleeding and mortality after Upper GI bleed - Initial score pre-endoscopy  Age  Shock: BP, pulse  Comorbidities - Final score post-endoscopy > Final Dx + evidence of recent haemorrhage  Active bleeding  Visible vessel  Adherent clot ``` Initial score ≥3 or final >6 are indications for surgery
60
Pathology of oesophageal varices
Portal HTN → dilated veins @ sites of porto-systemic anastomosis: L. gastric and inferior oesophageal veins
61
Causes of portal hypertension
Pre-hepatic: portal vein thrombosis Hepatic: cirrhosis (80% in UK), schisto (commonest worldwide), sarcoidosis. Post-hepatic: Budd-Chiari, RHF, constrict pericarditis
62
Management of oesophageal varices
- bleed prevention  1: β-B, repeat endoscopic banding  2: β-B, repeat banding, TIPSS (Transjugular Intrahepatic Porto-Systemic Shunt) - IR creates artificial channel between hepatic vein and portal vein → ↓ portal pressure.
63
Management of an Upper GI bleed
- Head-down - High flow oxygen + protect airway - 2 x 14G cannulae + IV bolus - Bloods: FBC, U+E (↑ urea), LFTs, clotting, x-match 6u, ABG, glucose - if remains shocked - o- blood - notify surgeons if severe IF VARICEAL BLEED - Terlipressin IV (splanchnic vasopressor)  Prophylactic Abx: e.g. ciprofloxacin 1g/24h Urgent endoscopy - Haemostasis of vessel or ulcer:  Adr injection; Thermal coagulation; Fibrin glue; Endoclips ``` Variceal bleeding:  2 of: banding, sclerotherapy, adrenaline, coagulation  Balloon tamponade ̄c  TIPSS ```
64
Indications for surgery after Upper GI bleed
 Re-bleeding  Bleeding despite transfusing 6u  Uncontrollable bleeding at endoscopy  Initial Rockall score ≥3, or final >6.
65
Risk factors for oesophageal cancer
- alcohol - smoking - achalasia - GORD - Fatty diet - Low vit A/C
66
Pathophysiology of oesophageal cancer
- 65% adenocarcinoma - lower 3rd | - 35% SCC - upper and middle 3rd
67
Presentation of oesophageal cancer
- Progressive dysphagia - weight loss - retrostrenal chest pain and dyspepsia - lymphadenopathy - hoarseness (recurrent laryngeal n invasion) - cough +/- aspiratino pneumonia - odonophagia - mets - jaunice, hepatomegaly, ascites
68
Ix for oesophageal cancer
OGD + biopsy - Bloods - Staging CT EUS - t stage
69
Staging used for oesophageal cancer
``` TMN T1 - submucosa T2 - muscularis propria T3 - adventitia T4 - adjacent structures ```
70
Causes of perforation
Inflammatory - chemical - PUD, Foreign body - infection - appendicitis, diverticulitis, meckels, cholecystitis, - ischaemia - mesenteric,, obstructive Ca, Bezoar, faeces - colitis - fistula, toxic megacolon Traumatic - iatrogenic - surgery. endoscopy - penetrating force - direct rupture - booerhavve/ mallory weiss
71
Ix for perforated GIT
- Blood - FBC, Amylase, CRP, clotting, ABG - urine dipstick - Erect CXR (erect 15min) - AXR - (riglers and psoas sign) - CT scan
72
Mx of Perforated PU
- A-E - NBM - fluid resuscitation - catheter +/- CVP line - analgesia - Abx - NGT +/- surgery is systemically unwell - abdominal washout and repair (patch - DU); may require gastrectomy
73
Ix for gastric outflow obstruction
- ABG - hypercholraemic hypokalaemic met alkalosis - AXR (dilated gastric air bubble air fluid level, collapsed distal bowel) - OGD
74
Rx for gastric outflow obstruction
- correct metabolic abnormalities - benign --> endscopic ballow dilation/ gastroenterostomy - malignant - stent/ resection
75
Risk factors for gastric cancer
- atrophic gastritis - pernicious anaemia, h.pylori) - diet high nitrates - smoking and alcohol - blood group A - low social class - familial - E cadherin abnormality - partial gastrectomy
76
Pathology of gastric cancer
Mainly adenocarcinomas, located on gastric antrum
77
Symptoms of gastric cancer
- weight loss + anorexia - dyspepsia - dysphagia - n + v
78
Signs of gastric cancer
- anaemia - epigastric mass - jaundice - ascites - hepatomegaly - virchow's node - acanthosis nigricans
79
Complications of gastric cancer
- perforation - upper Gi bleed - haematemesis, melaena - gastric outlet obstruction
80
Ix for gastric cancer
URGENT OGD + biopsy - CXR/USS/ CT - mets Staging - CT CAP
81
Complications of gastrectomy
- death - anastomotic leak - poor QoL - Vit B12 def - re-operation
82
describe the excretion of bilirubin
Hb → unconjugated to BR by splenic macrophages  uBR → cBR by BR-UDP-glucuronyl transferase in liver  Secreted in bile then cBR → urobilinogen (colourless)  Some urobilinogen is reabsorbed, returned to liver and re-excreted into bile.  Some reabsorbed urobilinogen is excreted into the urine  The urobilinogen that remains in the GIT is converted to stercobilin (brown) and excreted.
83
Causes of pre-hepatic jaundice
Excess BR production  Haemolytic anaemia  Ineffective erythropoiesis  e.g. thalassaemia
84
Causes of Hepatic jaundice
``` Unconjugated ↓ BR Uptake  Drugs: contrast, RMP  CCF ↓ BR Conjugation  Hypothyroidism  Gilbert’s (AD)  Crigler-Najjar (AR) Neonatal jaundice is both ↑ production + ↓ conjug. ``` ``` Hepatocellular Dysfunction  Congen: HH, Wilson’s, α1ATD  Infection: Hep A/B/C, CMV, EBV  Toxin: EtOH, drugs  AIH  Neoplasia: HCC, mets  Vasc: Budd-Chiari1 ```
85
Causes of post-hepatic jaundice
``` Obstruction  Stones  Ca pancreas  Drugs - OCP, sulfonylureas  PBC  PSC  Biliary atresia  Choledochal cyst  Cholangio Ca Inflammatory LN at porta hepatis - TB/ Ca Mirizzi's syndrome ```
86
Ix for Jaundice
- Urine  pre - No BR (acholuric); ↑ urobilinogen; ↑Hb if intravascular haemolysis  hepatic - ↑BR; ↑ urobilinogen  post- ↑↑BR; No urobilinogen - LFTs  pre - ↑uBR; ↑AST; ↑LDH  hepatic - ↑ cBR (usually); ↑AST:↑ALT; >2=EtOH/ <1=Viral; ↑ GGT (EtOH, obstruction); ↑ALP; Function: ↓ albumin, ↑ PT  post- ↑↑cBR; ↑AST,↑ALT; ↑↑ALP; ↑GGT - Other  pre - FBC and film, Coombs, Hb electrophoresis  hepatic - FBC, Ab, a1AT, Liver biopsy  post - Abdo US (dilated ducts >6mm), ERCP/MRCP; Ab
87
Causes of liver failure
- cirrhosis - acute  Infection: Hep A/B, CMV, EBV, leptospirosis  Toxin: EtOH, paracetamol, isoniazid, halothane  Vasc: Budd-Chiari  Other: Wilson’s, AIH  Obs: eclampsia, acute fatty liver of pregnancy
88
Signs of liver failure
```  Jaundice  Oedema + ascites  Bruising  Encephalopathy  Aterixis  Constructional apraxia (5-pointed star)  Fetor hepaticus Signs of cirrhosis / chronic liver disease ```
89
Ix for liver failure
``` Blood  FBC: infection, GI bleed, ↓ MCV (EtOH)  U+E - ↓U, ↑Cr: hepatorenal syndrome. Urea synth in liver -->poor test of renal function  LFT - AST:ALT > 2 = EtOH - AST:ALT < 1 = Viral - Albumin: ↓ in chronic liver failure - PT: ↑ in acute liver failure  Clotting: ↑INR  Glucose  ABG: metabolic acidosis  Cause: Ferritin, α1AT, caeruloplasmin, Abs, paracetamol levels ``` Microbiology  Hep, CMV, EBV serology  Blood and urine culture  Ascites MCS + SAAG Radiology  CXR  Abdo US + portal vein duplex
90
Pathophysiology and classification of hepatorenal syndrome
 Cirrhosis → splanchnic arterial vasodilatation → effective circulatory volume → RAS activation → renal arterial vasoconstriction.  Persistent underfilling of renal circulation → failure  Type 1: rapidly progressive deterioration (survival <2wks)  Type 2: steady deterioration (survival ~6mo)
91
Rx of hepatorenal syndrome
 IV albumin + splanchnic vasoconstrictors (terlipressin)  Haemodialysis as supportive Rx  Liver Tx is Rx of choice
92
Mx of liver failure
 Manage in ITU  Rx underlying cause: e.g. NAC in paracetamol OD  Good nutrition: e.g. via NGT ̄c high carbs  Thiamine supplements  Prophylactic PPIs vs. stress ulcers Monitor - fluids, bloods, glucose
93
Complications of liver failure
 Bleeding: Vit K, platelets, FFP, blood  Sepsis: tazocin (avoid gent: nephrotoxicity)  Ascites: fluid and salt restrict, spiro, fruse, tap, daily wt  Hypoglycaemia: regular BMs, IV glucose if <2mM  Encephalopathy: avoid sedatives, lactulose ± enemas, rifaximin  Seizures: lorazepam  Cerebral oedema: mannitol
94
Drugs to avoid prescribing in liver failure
opiates, oral hypoglycaemics, Na-containing IVI - Warfarin effects ↑ - Hepatotoxic drugs: paracetamol, methotrexate, isoniazid, salicylates, tetracycline
95
Poor prognostic factors in liver failure
```  Grade 3/4 hepatic encephalopathy  Age >40yrs  Albumin <30g/L  ↑INR  Drug-induced liver failure ```
96
Criteria for liver transplant
Kings college ``` Paracetamol-induced pH< 7.3 24h after ingestion Or all of: PT > 100s Cr > 300uM Grade 3/4 encephalopathy ``` ``` Non-paracetamol PT > 100s Or 3 out of 5 of: Drug-induced Age <10 or >40 >1wk from jaundice to encephalopathy PT > 50s BR ≥ 300uM ```
97
Pathophysiology of cirrhosis
Irreversible loss of hepatic architecture with bridging fibrosis and nodular regeneration
98
Signs of cirrhosis
``` Hands  Clubbing (± periostitis)  Leuconychia (↓ albumin)  Terry’s nails (white proximally, red distally)  Palmer erythema  Dupuytron’s contracture ``` Face  Pallor: ACD  Xanthelasma: PBC  Parotid enlargement (esp. ̄c EtOH due to dehydration increasing salvia production) Trunk  Spider naevi (>5, fill from centre)  Gynaecomastia  Loss of 2O sexual hair Abdo  Striae  Hepatomegaly (may be small in late disease)  Splenomegaly  Dilated superficial veins (Caput medusa)  Testicular atrophy Hyperdynamic circualtion
99
Complications of cirrhosis
- Decompensation --> heptatic failure (jaundice, encephalopathy, ↓Albumin, bruising (↑INR), hypoglycaemia) - Spontaneous bacterial peritonitis ``` - Portal hypertension Splenomegaly Ascites Varices - oeosphgeal, caput medusa, piles Encephalopathy ``` - ↑ risk of HCC
100
Ix to find cause of cirrhosis
```  EtOH: ↑MCV, ↑GGT  NASH: hyperlipidaemia, ↑ glucose  Infection: Hep, CMV, EBV serology  Genetic: Ferritin, α1AT, caeruloplasmin (↓ in Wilson’s)  Abs  Ca: α-fetoprotein ``` ``` Abdo US + PV Duplex  Small / large liver  Focal lesions  Reversed portal vein flow  Ascites - Ascitic Tap + MCS - PMN >250mm3 indicates SBP ``` Liver biopsy
101
Different Ab in cirrhosis
 AIH: SMA, SLA, LKM, ANA  PBC: AMA  PSC: ANCA, ANA  Ig: ↑IgG – AIH, ↑IgM – PBC
102
Mx of cirrhosis
``` Good nutrition EtOH abstinence Colestyramine for pruritus Screening  HCC: US & AFP every 3-6 m  Oesophageal varices: endoscopy +/- banding ``` Specific  HCV: Interferon-α  PBC: Ursodeoxycholic acid  Wilson’s: Penicillamine Decompensation  Ascites: fluid and salt restrict, spiro, fruse, tap, daily wt  Coagulopathy: Vit K, platelets, FFP, blood  Encephalopathy: avoid sedatives, lactulose ± enemas, rifaximin  Sepsis / SBP: tazocin (avoid gent: nephrotoxicity)  Hepatorenal syndrome: IV albumin + terlipressin
103
What is the Child-Pugh Grading score
Grades Cirrhosis  Predicts risk of bleeding, mortality and need for Tx ```  Graded A-C using severity of 5 factors  Albumin  Bilirubin  Clotting  Distension: Ascites  Encephalopathy ``` Score >8 = significant risk of variceal bleeding
104
Where are the portosystemic anastomoses
Oesophageal varices - Left and short gastric veins and Inf. oesophageal veins Caput medusae Peri-umbilical veins and Superficial abdo wall veins Haemorrhoids Sup. rectal veins and Inf. and mid. Rectal veins
105
Pathophysiology of Encephalopathy
 ↓Hepatic metabolic function  Diversion of toxins from liver directly into systemic system.  Ammonia accumulates and pass to brain where astrocytes clear it causing glutamate → glutamine  ↑ glutamine → osmotic imbalance → cerebral oedema
106
Classification of Encephalopathy
 1: Confused – irritable, mild confusion, sleep inversion  2: Drowsy – ↑ disorientated, slurred speech, asterixis  3: Stupor – rousable, incoherence  4: Coma – unrousable, ± extensor plantars
107
Presentation of encephalopathy
```  Asterixis, ataxia  Confusion  Dysarthria  Constructional apraxia  Seizures ```
108
Precipitants of encephalopathy
``` HEPATICS  Haemorrhage: e.g. varices  Electrolytes: ↓K, ↓Na  Poisons: diuretics, sedatives, anaesthetics  Alcohol  Tumour: HCC  Infection: SBP , pneumonia, UTI, HDV  Constipation (commonest cause)  Sugar (glucose) ↓: e.g. low calorie diet ```
109
Management of encephalopathy
20 degrees head up - Correct any precipitants  Avoid sedatives  Lactulose ± PO4 enemas to ↓ nitrogen-forming bowel bacteria → 2-4 soft stools/d  Consider rifaximin PO to kill intestinal microflora
110
Pathophysiology of ascites
Back-pressure → fluid exudation  ↓ effective circulating volume → RAS activation  (In cirrhosis: ↓ albumin → ↓ plasma oncotic pressure and aldosterone metabolism impaired)
111
Symptoms of ascites
Distension → abdominal discomfort and anorexia  Dyspnoea  ↓ venous return
112
Ix for ascites
Bloods: FBC, U+E, LFTs, INR, chronic hepatitis screen US: confirm ascites, liver echogenicity, PV duplex ``` Ascitic tap  MCS and AFB  Cytology  Chemistry: albumin, LDH, glucose, protein  SAAG = serum albumin – ascites albumin ``` Liver biopsy
113
Management of ascites
 Daily wt. aiming for ≤0.5kg/d reduction  Fluid restrict <1.5L/d and low Na diet  Spironolactone + frusemide (if response poor)  Therapeutic paracentesis ̄c albumin infusion (100ml 20% albumin /L drained) - Respiratory compromise - Pain / discomfort - Renal impairment  Refractory: TIPSS
114
Spontaneous bacterial peritonitis - causative organisms - Ix - management
- ascites and peritonitic abdomen  E. coli, Klebsiella, Streps Complicated by hepatorenal syn. in 30%  Ix: ascitic PMN > 250mm3 + MC+S  Rx: Tazocin or cefotaxime until sensitivities known  Prophylaxis: high recurrence - cipro long-term
115
Presentation of an alcoholic
 Fatty liver → hepatitits → cirrhosis  AST:ALT >2, ↑ GGT ``` GIT  Gastritis, erosions  PUD  Varices  Pancreatitis  Carcinoma ``` CNS  Poor memory / cognition  Peripheral polyneuropathy (mainly sensory)  Wernicke’s encephalopathy - Confusion; Ophthalmoplegia (nystagmus, LR palsy); Ataxia  Korsakoff’s: amnesia → confabulation  Fits, falls Heart  Arrhythmias: e.g. AF  Dilated cardiomyopathy  ↑BP Blood  ↑MCV  Folate deficiency →anaemia
116
Screening tool for alcoholics
``` CAGE  Cut down?  Annoyed by people’s criticisms  Guilty about drinking  Eye opener? ```
117
Features of alcohol withdrawal
0-72h after last drink  Consider in new ward pt (≤3d) ̄c acute confusion signs - Confusion, fits, hallucinations: esp formication (DTs) - ↑HR, ↓BP, tremor
118
Management of alcohol withdrawal
Tapering regimen of chlordiazepoxide PO / lorazepam IM Thiamine
119
Management of alcholism
 Group therapy or self-help (e.g. AA)  Baclofen: ↓ cravings  Acamprosate: ↓ cravings  Disulfiram: aversion therapy
120
Presentation of alcoholic hepatitis
```  Anorexia  D/V  Tender hepatomegaly  Ascites  Severe: Jaundice, bleeding, encephalopathy ```
121
Ix findings in alcoholic hepatitis
 Bloods: ↑MCV, ↑GGT, AST:ALT>2  Ascitic tap  Abdo US + PV duplex
122
Management of alcoholic hepatitis
```  Stop EtOH  Rx withdrawal  High dose B vitamins: Pabrinex  Optimise nutrition  Daily wt., LFT, U+E, INR  Mx complications of failure ```
123
Score that predicts mortality in alcoholic hepatitis
Maddrey score predicts mortality  Mild: 0-5% 30d mortality  Severe: 50% 30d mortality  1yr after admission: 40% mortality
124
Describe the different HBV Ab
 HBsAg +ve = current infection (>6mo = chronic disease)  HBeAg +ve = high infectivity  Anti-HBc IgM = recent infection  Anti-HBc IgG = past infection  Anti-HBs = cleared infection or vaccinated
125
Presentation of hepatitis B
Prodromal phase  Fever, malaise, arthralgia, nausea, anorexia  Distaste for cigarettes Icteric phase  Jaundice, HSM, lymphadenopathy, cholestasis ``` Extra-hepatic features due to immune complexes  Urticaria or vasculitic rash  Cryoglobulinaemia  PAN  GN  Arthritis ```
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Types of viral hepatitis, causes and how they are spread
``` A- FO Seafood, especially abroad B- IV Blood, body fluids, babies (vertical) C- IV Mainly blood. Less vertical cf. HCV D- IV Dependent on prior HBV infection E- FO Developing world ```
127
Management of viral hepatitis
A & E - supportive, avoid alcohol, +/- IFN α (fulminant hepatitis) B - supportive, avoid alcohol, +/- PEGinterferon α2b (chronic disease) C - PEGinterferon α2b + ribavirin
128
Risk factors for non-alcoholic fatty liver disease
 Obesity  HTN  T2DM  Hyperlipidaemia
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Presentation of NAFLD
 Mostly asymptomatic |  Hepatomegaly and RUQ discomfort may be present.
130
Ix and Mx for NAFLD
 BMI  Glucose, fasting lipids  ↑ transaminases: AST:ALT <1  Liver biopsy Mx -  Lose wt.  Control HTN, DM and lipids
131
Pathophysiology of NAFLD
``` ↑ Fat diet and ↓ exercise ↓ hepatic steatosis ↓ ↓ FAA ox and ↑ lipogenesis and ↑ lipid export ↕ Insulin resistance ```
132
What is Budd-Chiari syndrome and causes
Hepatic vein obstruction → ischaemia and hepatocyte damage → liver failure or insidious cirrhosis. - hypercoagulable - myeloproliferative, OCP, Anti-PL - Local tumour - HCC
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Presentation of Budd-Chiari syndrome
 RUQ pain: stretching of Glisson’s capsule  Hepatomegaly  Ascites: SAAG ≥1.1g/dL  Jaundice (and other features of liver failure)
134
Rx of Budd-Chiari syndrome
 Anticoagulate unless there are varices  Ascites: fluid and salt restrict, spiro, fruse, tap, daily wt  Other options: thrombolysis, angioplasty, TIPSS  Transplant if fulminant hepatic failure or cirrhosis  Rx underlying cause
135
Presentation of AI hepatitis
```  Cushingoid: hirsute, acne, striae  HSM  Fever/ malaise  Amenorrhoea  Polyarthritis  Pulmonary infiltration  Pleurisy ```
136
Presentation of PBC
```  Pruritus and fatigue  Pigmentation of face  Bones: osteoporosis, osteomalacia (↓ vit D)  Big organs: HSM  Cirrhosis and coagulopathy (↓ vit K)  Cholesterol ↑: xanthelasma, xanthomata  Steatorrhoea ``` Jaundice often occurs late
137
Pathology of PBC
Intrahepatic bile duct destruction by chronic | granulomatous inflammation → cirrhosis
138
Rx of PBC
Symptomatic  Pruritus: colestyramine, naltrexone  Diarrhoea: codeine phosphate  Osteoporosis: bisphosphonates Specific  ADEK vitamins  Ursodeoxcholic acid: ↓LFTs but no effect on mortality or need for transplant Liver transplant  End-stage disease or intractable pruritus  Recurrence occurs in ~20% but doesn’t usually → graft failure.
139
Pathophysiology of PSC
Inflammation, fibrosis and strictures and intra- and extra-hepatic ducts. Chronic biliary obstruction → secondary biliary cirrhosis → liver failure
140
Presentation of PSC
Symptoms  Jaundice  Pruritus and fatigue  Abdo pain Signs  Jaundice: dark urine, pale stools  HSM
141
Complications and associations of PSC
 Bacterial cholangitis  ↑ Cholangiocarcinoma  ↑ CRC ASSOCIATED UC - pANCA +ve
142
Rx of PSC
NEED TRANSPLANT  Pruritus: colestyramine, naltrexone  Diarrhoea: codeine phosphate  ADEK vitamins  Ursodeoxycholic acid improves cholestasis only  Abx for cholangitis  Endoscopic stenting for dominant strictures  Screening - Cholangiocarcinoma: US + Ca19-9 and CRC: colonoscopy
143
Signs and Symptoms of liver tumours
Symptoms  Benign tumours are usually asymptomatic  Systemic: fever, malaise, wt. loss, anorexia  RUQ pain: stretching of Glisson’s capsule  Jaundice is often late, except in cholangiocarcinoma  May rupture → intraperitoneal haemorrhage ``` Signs  Hepatomegaly: smooth or hard and irregular  Signs of chronic liver disease  Abdominal mass  Hepatic bruit (HCC) ```
144
Pathology of liver tumours
90% of liver tumours are 2O metastases  stomach, lung, colon, breast, uterus 90% of primary tumours are HCC.
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Causes and Mx of HCC
 Viral hepatitis  Cirrhosis: EtOH, HH, PBC  Aflatoxins (produced by Aspergillus) - resection - chemo, percutaneous ablation and embolization
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Causes of Cholangiocarcinoma
 Flukes (Clonorchis)  PSC  Congenital biliary cysts  UC
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Presentation and Mx of Cholangiocarcinoma
 Fever, malaise  Abdominal pain, ascites, jaundice  ↑BR, ↑↑ALP Mx - resect; pallative stent
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Indications for liver transplant in CLD
 Advanced cirrhosis |  HCC
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Contra- indications for liver transplant in CLD
```  Extra-hepatic malignancy  Severe cardiorespiratory disease  Systemic sepsis  HIV infection  Non-compliance ̄c drug therapy ```
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Complications of liver transplant
``` Acute rejection (T-cell mediated)  50% @ 5-10 days  Pyrexia, tender hepatomegaly  ↑ or change immunosuppressants  Sepsis  Hepatic artery thrombosis  CMV infection  Chronic rejection (6-9mo): shrinking bile ducts  Disease recurrence (e.g. HBV) ```
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Epidemiology of UC v CD
UC - 30s Smoking protective TH2-mediated CD - 20s Smoking ↑ risk TH1/TH17-mediated
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Macroscopic features of UC v CD
> UC Rectum + colon ± backwash ileitis Contiguous No Strictures > CD Mouth to anus esp. terminal ileum Skip lesions Strictures
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Microscopic features of UC v CD
``` > CD Transmural Inflammation Ulcers - Deep, thin, serpiginous → cobblestone mucosa Marked Fibrosis Granulomas Fistulae ``` > UC Mucosal Inflammation and Crypt Abscesses Ulcers - Shallow, broad Pseudoplyps
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Presentation of UC v CD
Fatigue, anorexia, malaise  +/- fever  Abdominal tenderness ``` UC  Diarrhoea  Blood ± mucus PR  Abdominal discomfort  Tenesmus, faecal urgency ``` ``` CD  Diarrhoea (not usually bloody)  Abdominal pain  Wt. loss  RIF mass,  Perianal abscess, fistulae, tag  anal/rectal stricture ```
155
Extra-intestinal features of IBD
``` Apthous ulcers Pyoderma gangrenosum Iritis Erythema nodosum Sacroilitis Arthralgia/AS Clubbing, Ca - Cholang, gall/renal stones ```
156
Complications of UC
```  Toxic megacolon - Diameter >6cm - Risk of perforation  Bleeding  Malignancy - CRC and Cholangiocarcinoma  Strictures → obstruction  Venous thrombosis ```
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Complications of CD
Fistulae - Entero-enteric/colonic → diarrhoea - Enterovesical → frequency, UTI - “pepperpot” anus Strictures → obstruction Abscesses  Abdominal  Anorectal ``` Malabsorption  Fat → Steatorrhoea, gallstones  B12 → megaloblastic anaemia  Vit D → osteomalacia  Protein → oedema ``` Toxic megacolon and Ca may occur (< cf. UC)
158
Ix findings in UC
 FBC: ↓Hb, ↑WCC  LFT: ↓albumin  ↑CRP/ESR  Blood cultures Stool  MCS: exclude Campy, Shigella, Salmonella, C.diff ``` Imaging  AXR: megacolon (>6cm), wall thickening  CXR: perforation  CT  Ba / gastrograffin enema - Lead-pipe: no haustra - Thumbprinting: mucosal thickening - Pseudopolyps: regenerating mucosal island ``` Ileocolonoscopy + regional biopsy (at least 2 from 5 sites)
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Classification of UC severity
Mild Fewer than 4 motions/ day; small amount of blood Moderate 4-6 motions/ day; mild-severe blood ``` Severe 6 + motions a day. Visible blood + 1 of: Pyrexia HR >90 Anaemia Erythrocyte sedimentation rate (mm/hour) > 30 ```
160
Management of acute severe UC
```  Resus: Admit, IV hydration, NBM  Hydrocortisone: IV 100mg QDS + PR; switch to oral when improve then taper (IV ciclosporin if CI)  Transfuse if required  Thromboprophylaxis: LMWH  Monitoring - Bloods: FBC, ESR, CRP, U+E - Vitals + stool chart - Twice daily examination - ± AXR ```
161
Medical management of UC
``` Inducing Remission - 5- ASAs (Mesalasine - Prednisolone +/- suppositories/enemas - Infliximab if steroid sparing ``` Maintaining remission 1) Sulfasalazine/mesalasine (PO/ Topical) 2) Azathioprine/ Mercaptopiurine PO 3) Inflixmab
162
Indications for emergency and elective surgery in UC/CD
 Toxic megacolon  Perforation  Massive haemorrhage  Failure to respond to medical Rx Elective - Chronic symptoms despite medical therapy - Carcinoma or high-grade dysplasia
163
Surgical management of UC - emergency - elective
Total / subtotal colectomy --> end ileostomy ± mucus fistula After ~3mo  Completion proctectomy + Ileal-pouch anal anastomosis (IPAA) or end ileostomy  Ileorectal anastomosis (IRA) Elective  Panproctocolectomy --> end ileostomy or IPAA  Total colectomy --> IRA
164
Complications after UC surgery
``` Abdominal  SBO  Anastomotic stricture  Pelvic abscess Stoma: retraction, stenosis, prolapse, dermatitis Pouch  Pouchitis (50%) (abdo pain, bloody diarrhoea, nausea) metronidazole + cipro  ↓ female fertility  Faecal leakage ```
165
Ix for CD
``` Bloods  FBC: ↓Hb, ↑WCC  LFT: ↓albumin  ↑CRP/ESR  Haematinics: Fe, B12, Folate  Blood cultures ``` Stool  MCS: exclude Campy, Shigella, Salmonella, C.diff Imaging  AXR: obstruction, sacroileitis  CXR: perforation  MRI - severity, pelvic disease and fistula  Small bowel follow-through or enteroclysis - Skip lesions - Cobblestoning: ulceration + mural oedema - String sign of Kantor: narrow terminal ileum Endoscopy  Ileocolonoscopy + regional biopsy
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Management of a severe CD attack
↑temp, ↑HR, ↑ESR, ↑CRP, ↑WCC, ↓albumin ```  Resus: Admit, NBM, IV hydration  Hydrocortisone: IV + PR if rectal disease (switch oral when can)  Abx: metronidazole PO or IV  Thromboprophylaxis: LMWH  Dietician Review - Elemental diet; Consider parenteral nutrition  Monitoring - Vitals + stool chart - Daily examination ``` No improvement --> methotrexate +/- infliximab
167
Medical management of CD
Inducing remission 1) Sulfasalazine 2) prednisolone 3) methotrxate 4) infliximab Maintaining remission 1) azathioprine or mercaptopurine 2) methotrexate 3) Infliximab / adalimumab
168
Indications for surgery in CD
Emergency  Failure to respond to medical Rx  Intestinal obstruction or perforation  Massive haemorrhage Elective  Abscess or fistula  Perianal disease  Chronic ill health  Carcinoma
169
Surgical management of CD | and its complications
 Limited resection: e.g. ileocaecal  Stricturoplasty  Defunction distal disease ̄c temporary loop ileostomy ``` Complications  Stoma complications  Enterocutaneous fistulae  Anastomotic leak or stricture  Short gut syndrome (Steatorrhoea ; ADEK and B12 malabsorption; Bile acid depletion → gallstones; Hyperoxaluria → renal stones) ```
170
Presentation of coeliac disease
GLIAD GI malabsorption - fatigue and weakness - n/v/d, abdo distension, colic, flatus, weight loss, steatorrhoea, vit def Lymphoma and carcinoma Immune associations - T1DM, IgA def Anaemia Dermatitis herpetiformis and apthous ulcers
171
Ix findings in coeliac disease
- Anaemia, ↓alb, vitamin def | - Anti-endomysial IgA Ab and anti-TTG IgG, Anti-gliadin
172
Definition of true and false diverticulum
Diverticulum is an outpouching of tubular structure - true - composed of complete wall - false - composed of only mucosa
173
Pathophysiology of diverticular disease
- Associated with raised intraluminal pressure (low fibre diet, no osmotic effect keeping stool wet) - mucosa herniates through muscularis propria at points of weakness where perforating arteries enter - most often sigmoid
174
Symptoms of diverticular disease
- altered bowel habit +/- left sided colic (relieved by defecation) - nausea - flatulence
175
Presentation of diverticulitis
- abdominal pain and tenderness (often LIF, localised peritonitis) - pyrexia
176
Pathophysiology of diverticulitis
- inspissated faeces --> obstruction of diverticulum
177
Complications of diverticulitis
- perforation (sudden onset chest pain, peritonitis and shock - air under diaphragm) - haemorrhage (PR bleed) - abscess (swinging fever, leukocytosis) - fistulae - strictures
178
Management of acute diverticulitis
- mild - bowel rest (fluids only) + co-amox - admit if unwell, cant tolerate fluids and uncontrolled pain medical - NBM - IV fluids - Analgesia - Abx - cefuroxime and metronidazole Surgery - if perforation haemorrhage, stricture/ obstruction - hartmanns / resection
179
Hinchley grading of perforation due to diverticulitis
1) small confined pericolic abscess 2) large abscess extending into pelvis 2) generalised purulent peritonitis 3) generalised faecal peritonitis
180
Symptoms of B3 (niacin) deficiency
Diarrhoea, Dermatitis, Dementia
181
Different types of gallstones
``` Cholesterol Stones: 20%  Large  Often solitary  Formation ↑ according to Admirand’s Trangle - ↓ bile salts - ↓ lecithin - ↑ cholesterol ``` Pigment Stones: 5%  Small, black, gritty, fragile  Calcium bilirubinate  Associated c¯ haemolysis Mixed Stones: 75%  Often multiple  Cholesterol is the major component
182
Risk factors for gallstones
```  Female  OCP, pregnancy  ↑ age  High fat diet and obesity  Racial: e.g. American Indian tribes  Loss of terminal ileum (↓ bile salts) ```
183
Complications of gallstones
In the Gallbladder 1. Biliary Colic 2. Acute cholecystitis ± empyema 3. Chronic cholecytsitis 4. Mucocele 5. Carcinoma 6. Mirizzi’s syndrome In the CBD 1. Obstructive jaundice 2. Pancreatitis 3. Cholangitis In the Gut 1. Gallstone ileus
184
Pathogenesis and presentation of biliary colic
Gallbladder spasm against a stone impacted in the neck of the gallbladder – Hartmann’s Pouch.  RUQ pain radiating → back (scapular region)  Assoc. c¯ sweating, pallor, n/v  Attacks may be ppted. by fatty food and last <6h  o/e may be tenderness in right hypochondrium  ± jaundice if stones passes in to CB
185
Differentials of biliary colic
Pancreatitis Cholecystitis Bowel Perforation
186
Ix for gallstone disease
 Urine: bilirubin, urobilinogen, Hb  Bloods: FBC, U+E, amylase, LFTs, G+S, clotting, CRP ``` Imaging  AXR: 10% of gallstones are radio-opaque - pneumobilia - gas froming infection  eCXR: look for perforation  US: - Stones: acoustic shadow - Dilated ducts: >6mm - Inflamed GB: wall oedema ```  If Dx uncertain after US - HIDA cholescintigraphy: shows failure of GB filling (requires functioning liver)  If dilated ducts seen on US → MRCP
187
Management of biliary colic
Conservative  Rehydrate and NBM  Opioid analgesia: morphine 5-10mg/2h max  High recurrence rate - surgical Rx favoured Surgical  As for conservative + either:  Urgent lap chole (same admission)  Elective lap chole @ 6-12wks
188
Differences between biliary colic, acute cholecystitis and Ascending cholangitis
All - RUQ Fever - Acute cholecystitis and ascending cholangitis Jaundice - Ascending cholangitis
189
Pathogenesis of acute cholecystitis
Stone or sludge impaction in Hartmann’s pouch |  → chemical and / or bacterial inflammation
190
Complications of acute cholecystitis
1. recurrence 2. Gangrene and rarely perforation 3. Chronic cholecystitis 4. Empyema
191
Symptoms and signs of Acute Cholecystitis
``` Symptoms  Severe RUQ pain - Continuous - Radiates to right scapula and epigastrium  Fever  Vomiting Signs  Local peritonism in RUQ  Tachycardia c¯ shallow breathing  ± jaundice  Murphy’s sign - 2 fingers over the GB and ask pt. to breath in → pain and breath catch. Must be –ve on the L ```
192
Management of acute cholecystitis
``` Conservative  NBM  Fluid resuscitation  Analgesia: paracetamol, diclofenac, codeine  Abx: cefuroxime and metronidazole  80-90% settle over 24-48h  Deterioration: perforation, empyema ``` Surgical  May be elective surgery @ 6-12wks (↓ inflam)  If <72h, may perform lap chole in acute phase Empyema  High fever  RUQ mass  Percutaneous drainage: cholecystostomy
193
Symptoms of chronic cholecystitis
``` Flatulent Dyspepsia  Vague upper abdominal discomfort  Distension, bloating  Nausea  Flatulence, burping  Symptoms exacerbated by fatty foods - CCK release stimulates gallbladder ```
194
Differentials of chronic cholecystitis
 PUD  IBS  Hiatus hernia  Chronic pancreatitis
195
Ix findings from chronic cholecystitis
 AXR: porcelain gallbladder |  US: stones, fibrotic, shrunken gallbladder
196
Mx of chronic cholecystitis
 Medical - Bile salts (not very effective)  Surgical - Elective cholecystectomy - ERCP first if US shows dilated ducts and stones
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What is a mucocele
Neck of gallbladder blocked by stone but contents remains sterile  Can be very large → palpable mass  May become infected → empyema
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What is Mirizzi's syndrome
Large stone in GB presses on the common hepatic duct → obstructive jaundice.  Stone may erode through into the ducts
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Pathogenesis, symptoms and mx of gallstone ileus
``` Large stone (>2.5cm) erodes from GB → duodenum through a cholecysto-duodenal fistula secondary to chonic inflam.  May impact in distal ileum → obstruction ``` ``` Symptoms Rigler’s Triad:  Pneumobiliia  Small bowel obstruction  Gallstone in RLQ ``` Mx - stone removal via enterotomy
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management of gallstones
``` Conservative  Monitor LFTs: passage of stone may → resolution  Vitamins ADEK  Analgesia  Cholestyramine ``` Interventional  If: no resolution, worsening LFTs or cholangitis  ERCP c¯ sphincterotomy and stone extraction Surgical  Open / lap stone removal c¯ T tube placement  T tube cholangiogram 8d later to confirm stone removal.  Delayed cholecystectomy to prevent recurrence
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Features of ascending cholangitis
Charcot’s triad: fever/rigors, RUQ pain, jaundice Reynolds pentad: Charcot’s triad + shock + confusion
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Management of ascending cholangitis
 Cef and met  1st: ERCP  2nd: Open or lap stone removal c¯ T tube drain
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Risk factors for pancreatic carcinoma
```  Smoking  Inflammation: chronic pancreatitis  Nutrition: ↑fat diet  EtOH  DM ```
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Pathology of pancreatic carcinoma
``` 90% ductal adenocarcinomas  Present late, metastasise early - Direct extension to local structures - Lymphatics - Blood → liver and lungs  60% located in head, 25% body, 15% tail ```
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Presentation of pancreatic carcinoma
 Typically male >60yrs  Painless obstructive jaundice: dark urine, pale stools  Epigastric pain: radiates to back, relieved sitting forward  Anorexia, wt. loss and malabsorption  Acute pancreatitis  Sudden onset DM in the elderly
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Signs of pancreatic carcinoma
 Palpable gallbladder  Jaundice  Epigastric mass  Thrombophlebitis migrans (Trousseau Sign)  Splenomegaly: PV thrombosis → portal HTN  Ascites
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Courvoisier’s Law
In the presence of painless obstructive jaundice, a | palpable gallbladder is unlikely to be due to stones.
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Ix for pancreatic carcinoma
Bloods: cholestatic LFTs, ↑Ca19-9 (90% sens), ↑Ca ``` Imaging  US: pancreatic mass, dilated ducts, hepatic mets, guide biopsy  EUS: better than CT/MRI for staging  CXR: mets  Laparoscopy: mets, staging ``` ERCP  Shows anatomy  Allows stenting  Biopsy of peri-ampullary lesions
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Rx of pancreatic carcinoma
``` Surgery  Fit, no mets, tumour ≤3cm (≤10% of pts)  Whipple’s pancreaticoduodenectomy  Distal pancreatectomy  Post-op chemo delays progression  5ys = 5-14% ``` Palliation  Endoscopic / percutaneous stenting of CBD  Palliative bypass surgery: – cholecystojejunostomy + gastrojejunostomy  Pain relief – may need coeliac plexus block
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Pathophysiology of acute pancreatitis
Pancreatic enzymes released and activated in vicious circle → multi-stage process. 1. Oedema + fluid shift + vomiting → hypovolaemic shock while enzymes → autodigestion and fat necrosis 2. Vessel autodigestion → retroperitoneal haemorrhage 3. Inflammation → pancreatic necrosis 4. Super-added infection: 50% of pts. c¯ necrosis
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Causes of acute pancreatitis
Aetiology  Gallstones (45%)  Ethanol (25%)  Trauma ```  Steroids  Mumps + Coxsackie B  Autoimmune: e.g. PAN  Scorpion (Trinidadian)  Hyperlipidaemia (I and V), ↑Ca, Hypothermia  ERCP: 5% risk  Drugs: e.g. thiazides, azathioprine ```  Idiopathic (20%): ?microstones
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Symptoms and signs of acute pancreatitis
``` Symptoms  Severe epigastric pain → back - May be relieved by sitting forward  Vomiting Signs  ↑HR, ↑RR  Fever  Hypovolaemia → shock  Epigastric tenderness  Jaundice  Ileus → absent bowel sounds  Grey Turners: flank  Cullens: periumbilical (tracks up Falciform) ```
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Criteria used for acute pancreatitis
Glasgow (IMRIE) - assess severity and predict mortality 1 = mild; 2 = mod; 3 = severe ``` PaO2 <8kPa  Age >55yrs  Neutrophils >15 x109/L  Ca2+ <2mM  Renal function U>16mM  Enzymes LDH>600iu/L AST>200 iu/L  Albumin <32g/L  Sugar >10mM ```
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Criteria for diagnosis of acute pancreatitis
- 2/3 1) CT 2) Amylase x 3 3) epigastric pain radiatating to back
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Ix findings in acute pancreatitis
``` Bloods  FBC: ↑WCC  ↑amylase (>1000 / 3x ULN) and ↑lipase - ↑ in 80% - Returns to normal by 5-7d  U+E: dehydration and renal failure  LFTs: cholestatic picture, ↑AST, ↑LDH  Ca2+: ↓  Glucose: ↑  CRP: monitor progress, >150 after 48hrs = sev  ABG: ↓O2 suggests ARDS ``` Urine: glucose, ↑cBR, ↓urobilinogen Imaging  CXR: ARDS, exclude perfed DU  AXR: sentinel loop, pancreatic calcification  US: Gallstones and dilated ducts, inflammation  Contrast CT: Balthazar Severity Score
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Conservative Mx of acute pancreatitis
Manage @ appropriate level: e.g. ITU if severe  Constant reassessment is key  Hrly TPR, UO  Daily FBC, U+E, Ca2+, glucose, amylase ABG Fluid Resuscitation - Aggressive fluid resus: keep UO >30ml/h - Catheter ± CVP Pancreatic Rest  NBM  NGT if vomiting  TPN may be required if severe to prevent catabolism Analgesia - Pethidine via PCA - Or morphine 5-10mg/2h max Antibiotics  Not routinely given if mild  Used if suspicion of infection or before ERCP  Penems often used: e.g. meropenem, imipenem OTHER - ARDS: O2 therapy or ventilation - EtOH withdrawal: chlordiazepoxide
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Interventional and surgical management for pancreatitis
ERCP + spincheterotomy --> If pancreatitis c¯ dilated ducts 2O to gallstones Surgery  Laparotomy + necrosectomy (pancreatic debridement)  Laparotomy + peritoneal lavage  Laparostomy: abdomen left open c¯ sterile packs in ITU
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Indications for surgery in acute pancreatitis
 Infected pancreatic necrosis  Pseudocyst or abscess  Unsure Dx
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Early complications of acute pancreatitis
``` Systemic  Respiratory: ARDS, pleural effusion  Shock: hypovolaemic or septic  Renal failure  DIC  Metabolic  ↓ Ca2+  ↑ glucose  Metabolic acidosis ```
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Late complications of acute pancreatitis
>1wk: Local  Pancreatic necrosis  Pancreatic infection  Pancreatic abscess - May form in pseudocyst or in pancreas --> Open or percutaneous drainage  Bleeding: e.g. from splenic artery --> May require embolisation  Thrombosis --> Splenic A., GDA or colic branches of SMA = May → bowel necrosis - Portal vein → portal HTN  Fistula formation --> Pancreato-cutaneous → skin breakdown
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What is a pancreatic pseudocysts and how is it managed
Collection of pancreatic fluid in the lesser sac surrounded by granulation tissue  4-6wks after acute attack  Persisting abdominal pain  Epigastric mass → early satiety ``` Complications  Infection → abscess  Obstruction of duodenum or CBD Ix --> Persistently ↑ amylase ± LFTs  DO US / CT ``` Rx  <6cm: spontaneous resolution  >6cm - Endoscopic cyst-gastrostomy OR Percutaneous drainage under US/CT
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Causes of Chronic Pancreatitis
``` AGITS  Alcohol (70%)  Genetic - CF  Immune - Lymphoplasmacytic sclerosing pancreatitis (↑IgG4)  Triglycerides ↑  Structural - Obstruction by tumour ```
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Presentation of Chronic Pancreatitis
Epigastric pain  Bores through to back  Relieved by sitting back or hot water bottle → erythema ab igne  Exacerbated by fatty food or EtOH Steatorrhoea and wt. loss DM: polyuria, polydipsia Epigastric mass: pseudocyst
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Ix for chronic pancreatitis
↑ glucose ↓ faecal elastase: ↓ exocrine function US: pseudocyst AXR: speckled pancreatic calcifications CT: pancreatic calcifications
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Management of acute pancreatitis
``` Diet  No EtOH  ↓ fat, ↑ carb Drugs  Analgesia: may need coeliac plexus block  Enzyme supplements: pancreatin (Creon)  ADEK vitamins  DM Rx Surgery - Indications  Unremitting pain  Wt. loss  Duct blockage --> Whipple’s/ endoscopic stenting ```
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Complications of chronic pancreatitis
```  Pseudocyst  DM  Pancreatic Ca  Pancreatic swelling → biliary obstruction  Splenic vein thrombosis → splenomegaly ```
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Differentials of upper abdominal pain
- cholecystitis (R) - pyelonephritis - uteric colic - hepatitis (R) - pneumonia - gastric ulcer (L)
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Differentials of RIF pain
```  appendicitis  Cholecystitis  Diverticulitis  Meckel’s diverticulitis  Cyst accident: torsion, rupture, haemorrhage  testicular torsion  Salpingitis / PID  Ruptured ectopic  Mesenteric adenitis  UTI  Crohn’s  Inguinal hernia ```
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Causes of LLQ pain
- ureteric colic - inguinal hernia - IBD - UTI - Gynaecological - testicular torsion - diverticulitis
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Causes of epigastic pain
- PUD - Cholecystitis - Pancreatitis - MI
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Causes of Peri-umbilical pain
- SI obstruction - LI obstruction - Appendicitis - AAA
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Features of carcinoid syndrome
FIVE HT  Flushing: paroxysmal, upper body ± wheals  Intestinal: diarrhoea  Valve fibrosis: tricuspid regurg and pulmonary stenosis  whEEze: bronchoconstriction  Hepatic involvement: bypassed 1st pass metabolism  Tryptophan deficiency → pellagra (3Ds)
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Pathogenesis of acute appendicitis
``` Obstruction of the appendix  Faecolith most commonly  Lymphoid hyperplasia post-infection  Tumour (e.g. caecal Ca, carcinoid)  Worms (e.g. Ascaris lumbicoides, Schisto) ``` Gut organisms → infection behind obstruction → oedema → ischaemia → necrosis → perforation  Peritonitis  Abscess  Appendix mass
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symptoms of acute appendicitis
Colicky abdo pain  Central (visceral irritation)→ localised in RIF ) parietal irritation)  Worse on movement  Anorexia  Nausea (vomiting is rarely prominent)  Constipation / diarrhoea
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Signs of appendicitis
```  Low-grade pyrexia: 37.5 – 38.5  ↑HR, shallow breathing  Foetor oris  Guarding and tenderness: @ McBurney’s point - +ve cough / percussion tenderness  Appendix mass may be palpable in RIF  Pain PR suggests pelvic appendix. Rovsing’s Sign  Pressure in LIF → more pain in RIF Psoas Sign  Pain on extending the hip: retrocaecal appendix ```
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Management of acute appendicitis
- Urine dip - Pregnancy test and exclude UTI - US - exclude gynae and visialise appendix - fluids - abx - cef + met - analgesia If uncertain - observe If certain - appendicetomy
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Complications of acute appendicitis
> Appendix Mass - Abx + NBM  Resolution of mass → interval appendicectomy  Exclude a colonic tumour: colonoscopy > Appendix Abscess  Mass enlarges, pt. deteriorates - Abx + NBM  CT-guided percutaneous drainage  If no resolution, surgery may involve right hemicolectomy. > Perforation - peritonitis
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Commonest causes of Small and Large bowel obstruction | - + a non-mechanical cause
``` SBO  Adhesions: 60%  Hernia  Neoplasm - mets/ lymphoma LBO  Colorectal Neoplasia: 60%  Diverticular stricture: 20%  Volvulus: 5% ``` - paralytic ileus
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Causes of paralytic ileus
```  Post-op - bowel handling/ anesthesia  Peritonitis  Pancreatitis/ localised inflammation  TCAs  Pseudo-obstruction  Metabolic: ↓K, ↓Na, ↓Mg, uraemia  Mesenteric ischaemia ```
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Presentation of SB v LB obstruction
SBO Early - Vom and mild distension. Late - Absolute constipation Colicky pain every 2-3 minutes LBO Early - Abdo pain and distension with absolute constipation Late - Vomiting and can be faeculant Colicky Pain every 10-15 minutes - constant pain --> strangulation
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Signs of bowel obstruction
```  ↑HR: hypovolaemia, strangulation  Dehydration, hypovolaemia  Fever- inflam disease or strangulation  Surgical scars  Hernias  Mass: neoplastic or inflammatory  Bowel sounds - ↑: mechanical obstruction - ↓: ileus  PR - Empty rectum; Rectal mass; Hard impacted stool; Blood from higher pathology ```
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Ix for bowel obstruction
Bloods  FBC: ↑WCC  U+E: dehydration, electrolyte abnormalities  Amylase: ↑↑ if strangulation/ perforation  VBG: ↑ lactate - strangulation  G+S, clotting: ?surgery Imaging  Erect CXR  AXR: ± erect film for fluid levels  CT: can show transition point Gastrograffin studies  Look for mechanical obstruction: no free flow  Follow through or enema  Follow through may relieve mild mechanical obstruction: usually adhesional Colonoscopy  Can be used in some cases  Risk of perforation  May be used therapeutically to stent
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Findings on AXR of SBO v LBO
SBO ≥3cm; central; Valvulae coniventes; many loops, and many, short fluid levels; LB Gas Absent LBO ≥6cm (caecum ≥9- emergency if ileocaecal valve working); Peripheral; Haustra; LB Gas Present; few loops; Few, long fluid levels
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medical management of bowel obstruction
 NBM  IV fluids: aggressive as pt. may be v. dehydrated  NGT: decompress upper GIT, stops vomiting, prevents aspiration  Catheterise: monitor UO  Analgesia: may require strong opioid  Antibiotics: cef+met if strangulation or perforation  Gastrograffin study: oral or via NGT  Consider need for parenteral nutrition  Regular clinical examination is necessary to ensure that the pt. is not deteriorating. - ↑ distension/ pain/ tenderness/ ↑ HR/ ↑RR  Repeat imaging and bloods
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Indications for surgery in bowel obstruction
 Closed loop obstruction  Obstructing neoplasm  Strangulation / perforation → sepsis, peritonitis  Failure of conservative Mx (up to 72h)
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Surgical management of. bowel obstruction
SBO: adhesiolysis LBO  Hartmann’s (proctosigmoidectomy)  Colectomy + 1° anastomosis + on table lavage  Palliative bypass procedure  Transverse loop colostomy or loop ileostomy  Caecostomy
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Types of stoma
Colostomy - flush to skin; LIF - loop --> entire loop of colon exteriorised and both proximal and distal end open into common stoma opening and are not transected - end --> created from proximal end of colon, distal end stapled/ sewn shut and remains as blind pouch Ileostomy; RIF; spout as enzymes toxic to skin - loop - Loop SI brought out, colon ann rectum removed - end - colon and rectum removed, and of ileum brought out
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Pathophysiology of a sigmoid volvulus and sign on AXR
 Long mesentery c¯ narrow base predisposes to torsion  Usually due to sigmoid elongation 2° to chronic constipation  ↑ risk in neuropsych pts.: MS, PD, psychiatric  Disease or Rx interferes c¯ intestinal motility → closed loop obstruction - coffee bean sign on AXR
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Mx of sigmoid volvulus
Sigmoidoscopy and flatus tube insertion 2) Sigmoid colectomy if Failed endoscopic decompression/ Bowel necrosis
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Presentation and Prevention of paralytic ileus
Presentation  Distension  Constipation ± vomiting  Absent bowel sounds ``` Prevention  ↓ bowel handling  Laparoscopic approach  Peritoneal lavage after peritonitis  Unstarched gloves ```
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Mx of paralytic ileus
 NBM  IV fluids: aggressive as pt. may be v. dehydrated  NGT: decompress upper GIT, stops vomiting, prevents aspiration  Catheterise: monitor UO Correct any underlying causes  Drugs  Metabolic abnormalities +/- parenteral nutrition
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What is obstruction and mx
Clinical signs of mechanical obstruction but no obstructing lesion found  Usually distension only: no colic - assoc elderly, CR disorders, hip arthroplasty and trauma Mx - neostigmine and colonoscopic decompressino
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Pathology and. Presentation of L v R colorectal carcinoma
ADENOCARCINOMA ``` Left  Altered bowel habit  PR mass (60%)  Obstruction (25%)  Bleeding / mucus PR  Tenesmus Right  Anaemia  Wt. loss  Abdominal pain ``` ``` Either  Abdominal mass  Perforation  Haemorrhage  Fistula ```
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Ix for colorectal carcinoma
Bloods  FBC: Hb - anaemia  LFTs: mets  Tumour Marker: CEA (carcinoembryonic Ag) (to monotor disease progression) ``` Imaging  CXR: lung mets  US liver: mets  CT and MRI (rectal and liver)- staging  Endoanal US: staging rectal tumours ``` Endoscopy + Biopsy  Flexi sig: 65% of tumours accessible  Colonoscopy
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Staging and grading of colorectal carcinomas
``` Dukes A Confined to bowel wall B Through bowel wall but no LNs C Regional LNs D Distant mets ``` ``` TNM  TIS: carcinoma in situ  T1: submucosa  T2: muscularis propria  T3: subserosa  T4: through the serosa to adjacent organs  N1: 1-3 nodes  N2: >4 nodes ``` Grade - low - high based on Dysplasia, mitotic index, hyperchromatism
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Surgical management of colorectal carcinomas
o R Hemicolectomy o Left Hemicolectomy o Sigmoidcolectomy (Sigmoid colon tumours) o Anterior Resection (High rectal tumours >5cm from the anus) o Abdominoperineal (AP) Resection (Low rectal tumours <5cm from the anus)
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Screening for colorectal carcinoma
FOB Testing  60-75yrs -  Home FOB testing every 2yrs: ~1/50 have +ve FOB  Colonoscopy if +ve: ~1/10 have Ca Flexi Sig  55-60yrs  Once only flexi Sig
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Risk factors for CRC
- FAP - age (>60yrs) - Fhx - IBD - ↓ fibre diet; ↑processed meat intake - smoking - ↑ alcohol intake.
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Presentation of mesenteric ischaemia
 Triad  Acute severe abdominal pain ± PR bleed  Rapid hypovolaemia → shock  No abdominal signs
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Causes of mesenteric ischaemia
 Arterial: thrombotic (35%), embolic (35%)  Non-occlusive (20%)  Splanchnic vasoconstriction: e.g. 2O to shock  Venous thrombosis (5%)  Other: trauma, vasculitis, strangulation
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Management of mesenteric ischaemia
- Fluids - Abx - LMWH - Laparotomy to resect necrotic bowel
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Presentation of Chronic Small Bowel Ischaemia
```  Severe, colicky post-prandial abdo pain  “gut claudication”  PR bleeding  Malabsorption  Wt. loss ``` Mx --> angioplasty
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Causes of Lower GI bleed
 Rectal: haemorrhoids, fissure  Diverticulitis  Neoplasm Other  Inflammation: IBD  Infection: shigella, campylobacter, C. diff  Polyps  Large upper GI bleed (15% of lower GI bleeds)  Angio: dysplasia, ischaemic colitis, HHT
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Mx of Lower GI bleed
 Resuscitate  Urinary catheter  Abx: if evidence of sepsis or perf  PPI: if upper GI bleed possible  Keep bed bound: need to pass stool may be large bleed → collapse  Stool chart  Diet: keep on clear fluids (allows colonoscopy)  Surgery: only if unremitting, massive bleed
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Pathophysiology of Haemorrhoids
Anal cushion: mass of spongy vascular tissue - Positioned @ 3, 7 and 11 O’clock  Where the 3 major arteries that feed the vascular plexuses enter the anal canal  Gravity, straining (+pregnancy, portal HTN) → engorgement and enlargement of anal cushions  Hard stool disrupts CT around cushions.  Cushions protrude and can be damaged by hard stool → bright red (capillary) bleeding.
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Classification of haemorrhoids
 1st degree: never prolapse  2nd: prolapse on defecation but spontaneously reduce  3rd: prolapse on defecation but require digital reduction  4th: remain permanently prolapsed
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Symptoms of haemorrhoids
```  Fresh painless PR bleeding - Bright red  Pruritis ani  Lump in perianal area  Severe pain = thrombosis ```
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Mx of haemorrhoids
 ↑ fibre and fluid intake  Stop straining @ stool Medical  Anusol: hydrocortisone  Topical analgesics  Laxatives: lactulose, Fybogel Interventional  Injection c¯ sclerosant - above dentate line - SE: impotence, prostatitis  Barron’s banding → thrombosis and separation - SE: bleeding, infection  Cryotherapy - SE: watery discharge post-procedure  Infra-red coagulation ``` Surgical: Haemorrhoidectomy  Excision of piles + ligation of vascular pedicles  Lactulose + metronidazole 1wk pre-op  Discharge c¯ laxatives post-op - SE: bleeding, stenosis ```
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Definition and causes of anal fissures
Tear of squamous epithelial lining in lower anal canal  Mostly trauma 2 ° to the passage of hard stool - Assoc. c¯ constipation - Spasm of internal anal sphincter contributes to pain and → ischaemia + poor healing  Crohn’s  Herpes  Anal Ca
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Presentation of anal fissures
```  Intense anal pain - Especially on defecation - May prevent pt. from passing stools - PR impossible  Fresh rectal bleeding ```
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Mx of anal fissures
 Soaks in warm bath  Toileting advice  Dietary advice: ↑ fibre and fluids ``` Medical  Laxatives: lactulose + fybogel  Topical → resolution in 75%  Lignocaine/ GTN/ Diltiazem  Botulinum injection ``` Surgical: Lateral partial sphincterotomy  Division of internal anal sphincter @ 3 O’clock - Complications  Minor faecal/flatus incontinence (= GTN)/ Perianal abscess
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Pathogenesis of Fistula in Ano
Abnormal connection between ano-rectal canal and the skin. - Usually occur 2° to perinanal sepsis - Blockage of intramuscular glands → abscess → discharges to form a fistula  Associations CD, Diverticular disease, Rectal Ca, Immunosuppression
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Goodsall's rule for Fistula's in Ano
Fistula anterior to anus track in a straight line (radial) Fistula posterior to anus always have internal opening at the 6 o’clock position → curved track
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Presentation, Rx and Mx of Fistula in Ano
Persistent anal discharge Perianal pain or discomfort - Endoanal USS/ MRI Mx - Low - Fistulotomy and excision --> Laid open to heal by 2° intention - High - a seton – passed through fistula and gradually tightened over months
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Pathogenesis of peri-anal abscess
 Anal gland blockage → infection → abscess E.g. coli, bacteroides  May develop from skin infections E.g. sebaceous gland or hair follicle OR Staphs
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Presentation of peri-anal abscess
Throbbing perianal pain - Worse on sitting Occasionally a purulent anal discharge Fluctuant mass on PR Septic signs: fever, tachycardia
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Rx of peri-anal abscess
Abx may suffice if Rx instigated v. early in course Most cases require EUA - I&D  Wound packed  Heals by 2O intention  Daily dressing for 7-10d
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Pathophysiology and risk factors of pilonidal sinus
Hair works its way beneath skin → foreign body reaction → formation of abscess  Usually occur in the natal cleft. Risk Factors  M>F=4:1  Geo: Mediterranean, Middle east, Asians  Often overweight c¯ poor personal hygiene (sweaty)  Occupations c¯ lots of sitting: e.g. truck drivers
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Presentation and Rx of pilonidal sinus
 Persistent discharge of purulent or clear fluid  Recurrent pain  Abscesses ``` Rx  Hygiene advice  Shave / remove hair from affected area  Incision and drainage of abscesses  Elective sinus excision ```
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Pathology and Presentation of anal carcinoma
 80% SCCs  Spread  Above dentate line → internal iliac nodes  Below dentate line → inguinal nodes Associated HPV Presentation  Perianal pain and bleeding  Pruritis ani  Faecal incontinence
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Ix and Rx of anal carcinoma
``` Ix  ↓ Hb (ACD)  Endoanal US  Rectal EUA + biopsy  CT / MRI: assess pelvic spread ``` Rx  Chemoradiotherapy: most pts  Surgery: reserved for  Tumours that fail to respond to radiotherapy  GI obstruction  Small anal margin tumours w/o sphincter involvement
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Rectal prolapse classification
Protrusion of rectal tissue through the anal canal. Type 1: Mucosal Prolapse  Partial prolapse of redundant mucosa Type 2: Full Thickness Prolapse ( elderly)
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Presentation of rectal prolapse
Mass extrudes from rectum on defecation  May reduce spontaneously or require manual reduction  May become oedematous and ulcerated → pain and bleeding  Faecal soiling  Assoc. c¯ vaginal prolapse and urinary incontinence ↓ sphincter tone on PR
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Rx of rectal prolapse
``` Partial Prolapse  Phenol injection  Rubber band ligation  Surgery: Delorme’s Procedure Complete Prolapse  Pelvic floor exercises/ Stool softeners  Rectopexy or Delorme’s Procedure ```
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Define a hernia
Protrusion of a viscus or part of a viscus through the walls of its containing cavity into an abnormal position
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Classification of Inguinal hernias
``` Indirect  80%: commoner in young  Congenital patent processus vaginalis  Emerge through deep ring  Same 3 coverings as cord and descend into the scrotum  Can strangulate ``` Direct  20%: commoner in elderly  Acquired ( ↑IAPe.g. Chronic cough/ constipation/ obesity)  Emerge through Hesselbach’s triangle  Can acquire internal and external spermatic fascia  Rarely descend into scrotum  Rarely strangulate
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Clinical features of Inguinal hernias
Children  Lump in groin which may descend into scrotum  Exacerbated by crying  Commonly obstruct Adults  Lump in groin, exacerbated by straining/cough  May be clear ppting event: e.g. heavy lifting  Dragging pain radiating to groin  May present c¯ obstruction/strangulation
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Mx of Inguinal hernia
Non-surgical  Rx RFs: cough, constipation  Lose weight  Truss Surgical  Tension-free mesh and suture repair
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Complications of inguinal hernias
``` Early  Haematoma / seroma formation: 10%  Intra-abdominal injury (lap)  Infection: 1%  Urinary retention ``` Late  Recurrence (<2%)  Ischaemic orchitis: 0.5%  Chronic groin pain / paraesthesia: 5%
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Femoral hernia pathology
Protrusion of viscus through femoral canal (bounded by femoral vein and lacunar ligament) into femoral triangle (inguinal ligament, adductus longus and sartorius) - more common in females due to shape of pelvis - acquires - increased intra-abdominal pressure
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Clinical features of a femoral hernia
Painless groin lump  inferior (and lateral) to the pubic tubercle.  Cough impulse.  Often irreducible (tight boarders) Commonly present - obstruction or strangulation  Tender, red and hot  Abdo pain, distension, vomiting, constipation
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Mx of femoral hernia
High risk of strangulation | Rx - herniotomy and heniorrhaphy
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Differntials of femoral hernia
- low inguinal hernia - femoral canal lipoma - femoral LN - saphena varix ( compressible, disappears when flat)
294
Definition and risk factors for incisional hernia
Hernia arises through a previously acquired defect - non- pulsatile, reducible soft and non-tender swelling near site of previous wound ``` Pre-operative  ↑ age  Obesity or malnutrition  Comorbidities: DM, renal failure, malignancy  Drugs: steroids, chemo, radio ``` ``` Intra-operative  Surgical technique/skill (major factor) -Too small suture bites - Inappropriate suture material  Incision type (e.g. midline)  Placing drains through wounds ``` Post-operative  ↑ IAP: chronic cough, straining, post-op ileus  Infection  Haematoma
295
Mx of incisional hernia
Conservative  Manage RFs: e.g. constipation, cough  Weight loss  Elasticated corset or truss ``` Surgical  Pre-Op - Optimise cardiorespiratory function - Encourage wt. loss  Nylon mesh repair: open or lap ```

IPE (9 decks)

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