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Year 3 Conditions > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

Define achalasia

A

a oesophageal motility disorder, characterised by loss of peristalsis and failure of the lower oesophageal sphincter (LOS)

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2
Q

Explain the aetiology / risk factors of achalasia

A

Degeneration of ganglion cells of the myenteric plexus in the oesophagus due to an unknown cause.

Oesophageal infection with Trypanosoma cruzi seen in Central and South America produces a similar disorder (Chagas’ disease).

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3
Q

Summarise the epidemiology of achalasia

A

Annual incidence: 1 in 100000.

Usual presentation age: 25–60 years.

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4
Q

Recognise the presenting symptoms of achalasia

A

Insidious onset and gradual progression of:

  • intermittent dysphagia involving solids and liquids;
  • difficulty belching;
  • regurgitation (particularly at night);
  • heartburn;
  • chest pain (atypical/cramping, retrosternal);
  • weight loss.
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5
Q

Recognise the signs of achalasia on physical examination

A

Signs of complications (e.g. cachectic)

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6
Q

Identify appropriate investigations for achalasia and interpret the results

A

1st Line:

  • Barium swallow: Dilated oesophagus which smoothly tapers down to the sphincter (beak- shaped).
  • Endoscopy: To exclude malignancy which can mimic achalasia.
  • Manometry:
  • -> Elevated resting LOS pressure (>45 mmHg);
  • -> incomplete LOS relaxation;
  • -> absence of peristalsis in the distal (smooth muscle portion) of the oesophagus.

Other Ix:

  • CXR: widened mediastinum, double right heart border (dilated oesophagus), an air-fluid level in the upper chest and absence of gastric bubble.
  • serology: for antibodies against T. cruzi
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7
Q

Define acute cholangitis

A

Infection of the bile duct; usually bacterial of duodenal source

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8
Q

Explain the aetiology / risk factors of acute cholangitis

A

Bile duct obstruction: usually caused by gall stones
- Can be benign structuring (tumour) or malignancy (pancreatic, gall bladder, bile duct)
- Iatrogenic: post-operative damage/altered structure of bile duct
Pathogenesis: increased pressure in bile duct brings bacteria in contact with blood, resulting in infection Risk Factors: age, female, cirrhosis

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9
Q

Summarise the epidemiology of acute cholangitis

A

15% have gallstones; 2-3% will develop acute cholangitis

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10
Q

Recognise the presenting symptoms of acute cholangitis

A

RUQ abdominal pain; fever, rigors, malaise

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11
Q

Recognise the signs of acute cholangitis on physical examination

A

Jaundice, RUQ tenderness
Charcot’s Triad: Abdominal pain, jaundice and fever (15-20% of cases)
Worsened condition => Reynold’s pentad (add septic shock and mental confusion)

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12
Q

Identify appropriate investigations for acute cholangitis and interpret the results

A

Bloods: FBC (raised WCC), CRP (raised); LFTs (obstructive picture: raised bilirubin, ALP), cultures
USS: distinguish between cholangitis and cholecystitis
MRCP: better imaging than USS
ERCP: gold standard test for biliary obstruction (but it is invasive)

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13
Q

Generate a management plan for acute cholangitis

A

Fluids, antiobiotics (ciprofloxacin, metronidazole), vasopressors

Unblock the bile duct: 24-48hrs after admission, once settled

  • ERCP (dilation of duct/removal of stones)
  • Lithotripsy: acoustic shock waves to break stones
  • Cholecystectomy: removal of gall bladder
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14
Q

Identify the possible complications of acute cholangitis and its management

A

Recurrent biliary pain; jaundice; further episodes; death risk increased

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15
Q

Summarise the prognosis for patients with acute cholangitis

A

Risk of death (multiple organ failure); 10-30% mortality

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16
Q

Define alcoholic hepatitis

A

Inflammatory liver injury caused by chronic heavy alcohol abuse

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17
Q

Explain the aetiology / risk factors of alcoholic hepatitis

A

One of three alcoholic liver diseases (hepatitis; steatosis; cirrhosis)
Histopathology: centrilobular ballooning, DEGENERATION AND NECROSIS OF HEPATOCYTES; STEATOSIS, neutrophilic inflammation, cholestasis

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18
Q

Summarise the epidemiology of alcoholic hepatitis

A

10-35% of heavy drinkers

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19
Q

Recognise the presenting symptoms of alcoholic hepatitis

A

May remain asymptomatic and undetected; mild illness with nausea, malaise, epigastric or right hypochondrial pain
More severe: jaundice, abdominal discomfort/swelling, swollen ankles, GI bleed

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20
Q

Recognise the signs of alcoholic hepatitis on physical examination

A

Excess Alcohol: malnourished, palmar erythema, Dupuytren’s contracture, facial telangiectasia, parotid enlargement, spider naevia, gynaecomastia, hepatomegaly
Alcoholic Hepatitis: febrile, tachycardic, jaundiced, bruising, encephalopathy (e.g. liver flap), ascites, hepatomegaly, splenomegaly

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21
Q

Identify appropriate investigations for alcoholic hepatitis and interpret the results

A

BLOODS: FBC (reduced Hb, platelets; increased MCV and WCC), LFT (increased transaminases, bilirubin, GGT, ALP, reduced albumin) U&Es ( urea and K+ low), Clotting (prolonged PT)
USS: for other causes
Upper GI endoscopy: investigate varices
Liver biopsy: distinguish other causes of hepatitis Electroencephalogram: indicative for encephalopathy

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22
Q

Generate a management plan for alcoholic hepatitis

A

ACUTE:
- Thiamine, VitC, monitor electrolytes and glucose
- Treat encephalopathy (lactulose)
- Ascites: diuretics (spironolactone and furosemide)
NUTRITION:
- Oral/NG feeding
- Avoid protein restriction unless encephalopathic
Steroid Therapy: Reduce short-term mortality
Long Term: see alcohol dependence

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23
Q

Identify the possible complications of alcoholic hepatitis and its management

A

Acute liver decompensation; hepatorenal syndrome; cirrhosis

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24
Q

Summarise the prognosis for patients with alcoholic hepatitis

A

10% mortality in 30 days, 40% in 1 year; most progress to cirrhosis with continued alcohol intake Maddrey’s discriminant factor: (bilirubin/17) + (PT prolongation x 4.6) [>32 = > 50% 30 day mortality) Glasgow Alcoholic Gepatitis score (GAHS) if >9, >50% 30 day mortality

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25
Q

Define anal fissure

A

A break or tear in the skin of the anal canal (usually posterior midline)

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26
Q

Explain the aetiology / risk factors of anal fissure

A

Stretching of the anal mucosa beyond capability.
HARD STOOLS, PREGNANCY, OPIATE ANALGESIA
- Constipation
- Passing large, hard stools
- Prolonged diarrhoea
- Childbirth trauma; sexual activity; Crohn’s Disease; Ulcerative Colitis
- Spasming of Internal Anal Sphincter: impaired blood supply to fissure, causing impaired healing
- STIs can cause breakdown of skin (syphilis, herpes)

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27
Q

Summarise the epidemiology of anal fissure

A

1:350; occur in 15-40 yrs, more common in men

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28
Q

Recognise the presenting symptoms of anal fissure

A

A tear or paper cut-like scar in the skin of the anal canal Pain on defecation

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29
Q

Recognise the signs of anal fissure on physical examination

A

Appearance of scar in midline, extending from the anal opening

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30
Q

Identify appropriate investigations for anal fissure and interpret the results

A

Investigate possible causes of fissure (proctoscopy, sigmoidoscopy or colonoscopy for CD or colorectal cancer)
DO NOT attempt DRE as it is painful

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31
Q

Generate a management plan for anal fissure

A

Non-surgical:
- gt ointment and lidocaine ointment, with diltiazem (calcium channel blocker)
- Topical anaesthetics, high-fiber diets and stool softeners
- 2nd line: botulinum toxin injection and topical diltiazem
Surgical: for those who have unsuccessfully tried non-surgical treatment for 1-3 months
- Lateral Sphincterectomy

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32
Q

Identify the possible complications of anal fissure and its management

A

Complications of treatment include Incontinence

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33
Q

Summarise the prognosis for patients with anal fissure

A

Most can be non-surgically treated

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34
Q

Define appendicectomy

A

Surgical removal of the vermiform appendix

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35
Q

Summarise the indications for an appendicectomy

A

acute appendicitis

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36
Q

Identify the possible complications of an appendicectomy

A

Wound infection, abscess, ileus

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37
Q

Contraindications of appendicectomy

A 
Haemodynamic instability
Lack of surgical expertise
Severe abdominal distension
Generalised peritonitis
Severe pulmonary disease
Pregnancy
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38
Q

Define amyloidosis

A

Extracellular deposition of amyloid fibrils; three types:

  • AL (light chain)
  • AA (serum A amyloid)
  • ATTR (familial)
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39
Q

Explain the aetiology / risk factors of amyloidosis

A

Amyloid fibril deposition disrupts the structure and function of normal tissue; amyloidosis is classified according to fibril subunit:

  • AL – monoclonal immunoglobulin light chains; associated with plasma cell disorders i.e. multiple myeloma
  • AA – Serum amyloid protein A; associated with chronic inflammatory conditions (IBD and rheumatoid arthritis)
  • ATTR – a genetic variant; autosomal dominant transmitted mutations
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40
Q

Summarise the epidemiology of amyloidosis

A

Primary - AL Amyloidosis: 3-600 annual cases
Secondary - AA Amyloidosis: 1-5% of those with chronic inflammatory conditions
Hereditary Amyloidosis: 5% of patients with systemic amyloidosis

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41
Q

Recognise the presenting symptoms of amyloidosis

A

Multi-systemic affects:

  • Renal: renal failure, oedema
  • Vascular: Periorbital Purpura
  • PNS: pain/numbness in arms and legs
  • GI: macroglossia, bleeding, weight loss, malabsorption
  • Cardiac: angina, orthopnoea, PND
  • Haematological: bleeding diathesis
  • Neurological: carpal tunnel syndrome
  • Dermatological: waxy skin, easy bruising
  • Joints: painful joints
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42
Q

Recognise the signs of amyloidosis on physical examination

A

Multi-systemic Affects:

  • Renal: proteinuria
  • Cardiac: arrhythmias, heart failure
  • GI: hepatosplenomegaly
  • Neurological: sensory and motor neuropathy
  • Skin: purpura around eyes
  • Joints: tender, swelled joints
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43
Q

Identify appropriate investigations for amyloidosis and interpret the results

A

Tissue biopsy: congo red stain; to diagnose AA; poor diagnostic power for AL

Urine: proteinuria, free immunoglobulin light chains for AL
Blood: CRP, ESR, rheumatoid factor, LFTs, U&Es

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44
Q

Define appendicitis

A

Inflammation of the appendix

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45
Q

Explain the aetiology / risk factors of appendicitis

A

Organisms of the gut invade the appendix

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46
Q

Summarise the epidemiology of appendicitis

A

very common

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47
Q

Recognise the presenting symptoms of appendicitis

A

pain in the umbilical region that migrates to the right iliac fossa region
Diarrhoea/constipation
Anorexia and vomiting (rare)

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48
Q

Recognise the signs of appendicitis on physical examination

A

Rovsing’s sign: pushing down on the LIF causes an increase in pain in the RIF
Psoas sign: pain on extending the hip
Cope sign: pain on flexion and internal rotation of the right hip
Rebound tenderness: when infection involves the peritoneum

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49
Q

Identify appropriate investigations for appendicitis and interpret the results

A

FBC: CRP, neutrophil leucocytosis
CT: high diagnostic accuracy (reduces –ve appendicectomy, but can cause delay)
USS: appendix not always visualised

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50
Q

Generate a management plan for appendicitis

A

Prompt appendicectomy

Antibiotics: metronidazole and cefuroxime

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51
Q

Identify the possible complications of appendicitis and its management

A

Perforation: more common if feacolith is present; young children
Appendix Mass: when inflamed appendix becomes covered in omentum (US/CT helps with diagnosis)
Appendix Abscess: can result in appendix mass also

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52
Q

Summarise the prognosis for patients with appendicitis

A

Most recover easily after surgery, between 10-28 day recovery

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53
Q

Define autoimmune hepatitis

A

Chronic hepatitis of unknown aetiology; characterised by autoimmune features, hyperglobulinaemia and the presence of circulating antibodies

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54
Q

Explain the aetiology / risk factors of autoimmune hepatitis

A

Genetically predisposed individual – environmental agent leads to hepatocyte expression of HLA antigens, which become focus of t-cell mediated attack
Type 1 (classic): ANA, anti-smooth muscle antibodies (ASMA), anti-actin antibodies (AAA), anti-soluble liver antigen (anti-SLA)
Type 2: antibodies to liver/kidney microsomes

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55
Q

Summarise the epidemiology of autoimmune hepatitis

A

Type 1: all age groups (mainly young women)

Type 2: generally disease of girls and young women

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56
Q

Recognise the presenting symptoms of autoimmune hepatitis

A 
May be asymptomatic and discovered incidentally by deranged LFTs
Insidious Onset: malaise, fatigue, anorexia, weight loss, nausea, jaundice, amenorrhoea, epistaxis
Acute Hepatitis (25%): RUQ pain, fever, anorexia, jaundice, nausea, vomiting, diarrhoea
Family history of autoimmune disease (e.g. T1DM, vitilgo)
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57
Q

Recognise the signs of autoimmune hepatitis on physical examination

A

Chronic Liver Disease Signs: spider naevi, gynacomastea, abnormal hair growth
Late Features: Ascites; oedema and encephalopathy
Cushingoid Features: round face, cutaneous striae, acne, hirsuitism

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58
Q

Identify appropriate investigations for autoimmune hepatitis and interpret the results

A

Bloods: LFTs (increase AST, GGT, ALT, AlkPhos, bilirubin)
Clotting (increase PT)
FBC (mild reduced Hb and platelets and WCC- hypersplenism in portal hypertension)
Liver Biopsy: needed for diagnosis; interface hepatitis or cirrhosis
Other: to rule out other causes e.g. viral serology, ferritin/trasnferritin
USS/CT/MRI: of liver and abdomen: visualise lesions
ERCP: rule out Primary Sclerosing Cholangitis

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59
Q

Define Barrett’s oesophagus

A

a change in the normal squamous epithelium of the oesophagus to specialised intestinal metaplasia.
[Metaplasia of the squamous epithelium of the lower third of the oesophagus to columnar epithelium]

Mucosal inflammation and erosion, and replacement of mucosa with metaplastic columnar epithelium, in the lower third of the oesophagus.
Presence of goblet cells is necessary for diagnosis

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60
Q

Explain the aetiology / risk factors of Barrett’s oesophagus

A

Chronic inflammation: principal cause is GORD

RF: acid or bile reflux/GORD, male sex, age, white, family history of BO or oesophageal adenocarcinoma, obesity, smoking

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61
Q

Summarise the epidemiology of Barrett’s oesophagus

A

Men are 8x more at risk

Caucasian is at a higher risk

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62
Q

Recognise the presenting symptoms of Barrett’s oesophagus

A

Frequent heartburn, dysphagia, haematemesis, retrosternal pain, weight loss

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63
Q

Recognise the signs of Barrett’s oesophagus on physical examination

A

Diagnosis made in imaging

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64
Q

Identify appropriate investigations for Barrett’s oesophagus and interpret the results

A

Upper GI endoscopy with biopsy

barium oesophagram

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65
Q

Generate a management plan for Barrett’s oesophagus

A

If pre-malignant/high-grade dysplasia – oesophageal resection or eradicative mucosectomy

If no pre-malignancy or high-grade dysplasia: endoscopic surveillance + biopsy; every 1-3 years
- Anti-reflux measures: PPIs (omeprazole)

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66
Q

Identify the possible complications of Barrett’s oesophagus and its management

A

high risk of oesophageal cancer (oesophagogastric junctional adenocarcinoma)

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67
Q

Summarise the prognosis for patients with Barrett’s oesophagus

A

Risk of cancer is 1-7:1000; those with oesophageal cancer have low survival rates (most are <1 year)

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68
Q

Define cholecystitis

A

inflammation of the gallbladder

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69
Q

Explain the aetiology / risk factors of cholecystitis

A

Inflammation of the gallbladder – most commonly by gallstones. But can occur with blockage due to tumour or scarring

Risk Factors: age, female, pregnancy, oral contraceptives, obesity, diabetes mellitus

Calculous Cholecystitis: gallstones blocking flow; gallbladder can become infected (E. coli, Klebsiella). Can spread to diaphragm
Acalculous Cholecystitis: no stones; vasculitis, chemotherapy, major trauma or burns
Chronic Cholecystitis: repeated inflammations; may be asymptomatic

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70
Q

Summarise the epidemiology of cholecystitis

A

Accounts for 3-10% of abdominal pain; highest in 50-69 year olds

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71
Q

Recognise the presenting symptoms of cholecystitis

A

RUQ pain, worse on eating fatty foods, nausea and vomiting. Biliary colic preceding cholecystitis

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72
Q

Recognise the signs of cholecystitis on physical examination

A

Fever, tender abdomen, palpable gallbladder, jaundice

Murphy’s Sign: while pressing on RUQ, pain on inspiration and breath is terminated

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73
Q

Identify appropriate investigations for cholecystitis and interpret the results

A

Bloods: FBC (increased WCC), CRP (elevated), bilirubin (elevated)
USS: of RUQ, most commonly used to diagnose
CT: if complications (perforation, gangrene) are suspected

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74
Q

Generate a management plan for cholecystitis

A

Surgery: laparoscopic cholecystectomy (early has better prognosis)

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75
Q

Identify the possible complications of cholecystitis and its management

A

Gangrene, gallbladder rupture (abscess, peritonitis), empyema, fistula formation, gallstone ileus

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76
Q

Summarise the prognosis for patients with cholecystitis

A

Pre-complication prognosis is better, 25-30% develop complications

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77
Q

Define cirrhosis

A

End stage of chronic liver damage with replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes.

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78
Q

What is decompensated liver failure and what are the symptoms?

A

Compensated: Np symptoms of the disease
Decompensated: cirrhosis has progressed to the point that the liver is having trouble functioning and you start having symptoms of the disease

jaundice, ascites, encephalopathy or GI bleeding

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79
Q

Explain the aetiology / risk factors of cirrhosis

A

Most common: chronic alcohol misuse
Chronic viral hepatitis: Hep B+C most common worldwide
Autoimmune hepatitis
Drugs: e.g. methotrexate, hepatotoxic drugs
Inherited: α1-Antitrypsin deficiency, haemochromatosis, Wilson’s disease, galactosaemia, CF
Vascular: Budd-Chiari syndrome
Chronic biliary diseases: primary biliary cirrhosis, PSC, biliary atresia
Cryptogenic: 5-10%
Non-alcoholic steatohepatitis (NASH): associated with obesity, diabetes, parenteral nutrition, and drugs (amiodarone, tamoxifen)
Decompensation: infection, GI bleeding, constipation, alcohol, drugs

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80
Q

Summarise the epidemiology of cirrhosis

A

Top 10 causes of death

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81
Q

Recognise the presenting symptoms of cirrhosis

A

Early and non-specific: anorexia, nausea, fatigue, weakness, weight loss
Symptoms (decreased synthetic function): easy bruising, abdominal swelling, ankle oedema
Symptoms (reduced detoxification): jaundice, personality changes, altered sleep patterns, amenorrhoea
Symptoms (Portal Hypertension): abdominal swelling, haematemesis, PR bleeding or melaena

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82
Q

Recognise the signs of cirrhosis on physical examination

A

Chronic Liver Disease: ABCDE

  • Asterixes (liver flap)
  • Bruises
  • Clubbing
  • Dupuytren;s Contracture
  • Erythema
  • Other: jaundice, gynaecomastia, leukonychia, spider naevia, scratch marks, ascites, hepatomegaly, caput medusa, splenomegaly
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83
Q

Identify appropriate investigations for cirrhosis and interpret the results

A

BLOODS: FBC (lowered Hb, platelets [hypersplenism]) LFTs (can be normal, increased AlkPhos, reduced albumin) Clotting (prolonged PT), Serum AFP
Other: to determine cause (serology, α1 antitrypsin, caeruloplasmin {Wilson’s Disease])
Liver Biopsy: percutaneous (trans jugular if ascites or clotting deranged)
Imaging: USS, CT, MRI (detect complications, hepatocellular carcinoma, thrombosis), MRCP
Endoscopy: examine for varices
Child-Pugh Grading: Class A/B/C depending on score

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84
Q

Generate a management plan for cirrhosis

A

Treat cause if possible
Advice: avoid alcohol, sedatives, opiates, NSAIDs and drugs that affect the liver, ensure good nutrition Treat complications:
- Encephalopathy: treat infections, exclude GI bleed, lactulose
- Ascites: diuretics (spironolactone/furosemide), sodium restriction, fluid restriction
- Spontaneous Bacterial Peritonitis: antibiotic treatment (cefuroxime and metronidazole)
- Surgical: insertion of TIPS (relieve portal hypertension). Liver transplant

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85
Q

Identify the possible complications of cirrhosis and its management

A

Portal hypertension with ascites, encephalopathy or variceal haemorrhage, SBP, hepatocellular carcinoma, peritonitis
Renal failure

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86
Q

Summarise the prognosis for patients with cirrhosis

A

Depends on aetiology: generally poor. 5 year survival at 50%, with ascites 2 year survival at 50%

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87
Q

Define coeliac disease

A

Inflammatory disease caused by intolerance to gluten, causing chronic intestinal villous atrophy and malabsorption

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88
Q

Explain the aetiology / risk factors of coeliac disease

A

Sensitivity to the gliadin component of the cereal protein, gluten – triggers an immunological reaction in the small intestine leading to mucosal damage and loss of villi
10% risk of first relatives being affected

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89
Q

Summarise the epidemiology of coeliac disease

A

1:2000; more common in western society

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90
Q

Recognise the presenting symptoms of coeliac disease

A

pain, tiredness,

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91
Q

Recognise the signs of coeliac disease on physical examination

A

Anaemia: pallor
Malnutrition: short stature, abdominal distension, wasted buttocks in children
Vitamin/Mineral Deficiencies: osteomalcia, easy bruising
Intense itchy blisters on elbows/knees/buttocks

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92
Q

Identify appropriate investigations for coeliac disease and interpret the results

A

Bloods: FBC, iron, folate, U&Es, albumin, Ca2+ and phosphate
Serology: testing for IgG anti-glandin, tissue transglutaminase (tTG)
Stool: culture to exclude infection
D-xylose test: reduced urinary excretion after oral xylose (small bowel malabsorption)
Endoscopy: direct visualisation shows villous atrophy in small intestine (jejenum and ileum), giving smooth, flat appearance to mucosa.
Biopsy: villous atrophy with crypt hyperplasia of duodenum

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93
Q

Generate a management plan for coeliac disease

A

Advice: Withdrawal of gluten from the diet and educating on dietary advice
Medical: vitamin and mineral supplements

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94
Q

Identify the possible complications of coeliac disease and its management

A

Iron, folate and vitamin B12 deficiencies; osteomalacia; ulcerative jejunoileitis; bacterial overgrowth

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95
Q

Summarise the prognosis for patients with coeliac disease

A

With strict adherence, most patients make a full recovery; symptoms resolving in weeks
Life-long diet changes need to be made

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96
Q

Define Crohn’s disease

A

Chronic granulomatous inflammatory disease that can affect any part of the GI tract.
Most commonly in ileum and colon

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97
Q

Explain the aetiology / risk factors of Crohn’s disease

A

Combination of environmental factors and genetic predisposition
Genetics: siblings are 30x more likely to develop it;
Immune system: impaired innate immunity
Environmental Factors: smoking, oral contraceptives,

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98
Q

Summarise the epidemiology of Crohn’s disease

A

5-8:100,000; lower incidence in Asia and east Africa; bimodal onset at 15-30 and 60-80 years

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99
Q

Recognise the presenting symptoms of Crohn’s disease

A

Crampy abdominal pain; diarrhoea; fever/malaise/weight loss; symptoms of complications

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100
Q

Recognise the signs of Crohn’s disease on physical examination

A

Weight loss; clubbing; anaemia signs
Aphthous ulceration of the mouth
Perianal skin tags, fistulae and abscesses
Signs of complications (eyes, joints or skin)

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101
Q

Identify appropriate investigations for Crohn’s disease and interpret the results

A

Blood: FBC, U&Es, LFTs, ESR, CRP (p-anca negative)
Stool microscopy and culture: exclude infective colitis
AXR: toxic megacolon
Erect CXR: to see perforation
Small-bowel barium follow-through; reveal fibrosis/strictures, rose thorn appearance
Endoscopy (OGD, colonoscopy) and biopsy: differentiate between CD and UC. Will see granulomas in CD.

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102
Q

Generate a management plan for Crohn’s disease

A 
Acute Exacerbation:
- Fluid rescus
- IV or oral corticosteroids
- 5-ASA Analogues (e.g. mesalazine)
- Analgesia
- Monitor activity markers
Long Term:
- Steroids: to treat acute exacerbations
- 5-ASA analgoues (e.g. mesalazine) to reduce relapses
- Immunosuppression: steroid-sparing agents (e.g. azathioprine) to reduce relapse
- Anti-TNF agents (e.g. infliximab) to achieve and maintain remission
Advice:
- Stop smoking
- Dietician referral
- Education and advice
Surgery:
- Indicated by failure of medical treatment, failure to thrive in children or complications
- Resection of bowel and stoma formation
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103
Q

Identify the possible complications of Crohn’s disease and its management

A

GI: Haemorrhage, bowel obstruction, perforation, fistulae, GI carcinoma
Extra intestinal: uveitis; episcleritis; gallstones; kidney stones

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104
Q

Summarise the prognosis for patients with Crohn’s disease

A

Chronic relapsing condition; two thirds will require surgery eventually, and two thirds of these will have >1 procedure.

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105
Q

Define diverticular disease

A

Diverticulosis: presence of diverticulae outpouchings of the colonic mucosa and submucosa throughout the large bowel
Diverticular Disease: diverticulosis associated with complications (e.g haemorrhage, infection) Diverticulitis: acute inflammation and infection of the colonic diverticulae

Hinchey Classification:

  • Ia: phlegmon
  • Ib and II: localised abscesses
  • III: perforation with purulent peritonitis
  • IV: faecal peritonitis
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106
Q

Explain the aetiology / risk factors of diverticular disease

A

A low fibre diet can lead to loss of stool bulk, consequently high pressures are required to expel the stool, leading to herniations through the muscularis at weak points
Pathogenesis: most common in sigmoid colon; can be obstructed with stool, leading to bacterial overgrowth, injury and diverticulitis

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107
Q

Recognise the presenting symptoms of diverticular disease

A 
Often asymptomatic (80-90%)
Complications: PR bleeding, diverticulitis (LIF pain, fever) diverticular fistulation into the bladder (pneumaturia, faecaluria and recurrent UTIs)
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108
Q

Recognise the signs of diverticular disease on physical examination

A

Diverticulitis: tender abdomen, signs of local/generalised peritonitis if perforation occurred

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109
Q

Identify appropriate investigations for diverticular disease and interpret the results

A

Bloods: FBC, clotting, cross-match
Barium Enema: demonstrated presence of diverticulae (not in acute; risk of perforation) Flexible sigmoidoscopy and colonoscopy: diverticulae can be seen
Acute Setting: CT

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110
Q

Generate a management plan for diverticular disease

A

Asymptomatic: soluble, high-fibre diet. [Anti-inflammatories (mesalazine) under investigation as preventions]
GI Bleed: managed conservatively
- IV hydration
- Bowel rest
Surgery: may be necessary with recurrent attacks or complications
- Open or laparoscopic approaches
- Open Hartmann’s (resection and stoma)
- One-Stage resection and anastomosis
- Laparoscopic drainage, peritoneal lavage and drain replacement can be effective

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111
Q

Identify the possible complications of diverticular disease and its management

A

Diverticulitis, pericolic abscess, perforation, faecal peritonitis, colonic obstruction, fistula formation, haemorrhage

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112
Q

Summarise the prognosis for patients with diverticular disease

A

10-25% will have >1 episode of diverticulitis

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113
Q

Define gallstones and biliary colic

A

presence of solid concretions in the gallbladder. Gallstones form in the gallbladder but may exit into the bile ducts.
Symptoms ensue if a stone obstructs the cystic, bile, or pancreatic duct.

Biliary colic is right upper quadrant pain, radiating to shoulder

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114
Q

Explain the aetiology / risk factors of gallstones and biliary colic

A

gallstones: 90% are made of cholesterol. form in the gall bladder, but can move into the ducts, where they can cause symptoms

BC: Obstruction of common bile duct/cystic duct by a gall stone. Acute pain can be exacerbated by certain foods (high in fat)

Risk Factors: age, female, family history, increased oestrogen exposure (pregnancy, birth control) diabetes mellitus, obesity, rapid weight loss, FHx

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115
Q

Summarise the epidemiology of gallstones and biliary colic

A

high prevalence, usually symptomatic

2-3% risk of developing biliary colic

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116
Q

Recognise the presenting symptoms of gallstones and biliary colic

A

Gallstones are highly prevalent, but most (80%) are asymptomatic.
Pain: sharp RUQ pain, radiating to right shoulder/back, can follow high fat meals, lasts 30-120 minutes, nausea, vomiting,

Other presentations
Biliary colic: is characterised by steady, severe pain (intensity >5 on a scale of 1-10) in the right upper quadrant (RUQ) of the abdomen lasting more than 15-30 minutes. An attack of simple biliary colic commonly requires an analgesic but should resolve within 5 hours.
Cholecystitis: biliary pain lasting more than 5 hours is accompanied by features of inflammation: fever, marked RUQ tenderness (Murphy’s sign), and leukocytosis. Some patients progress to sepsis. Occasionally, stones can perforate the gallbladder, leading to intestinal obstruction (gallstone ileus).
Choledocholithiasis: when stones obstruct the bile ducts, biliary-type pain is accompanied by cholestasis, which manifests as jaundice. More sinister is acute cholangitis, characterised by Charcot’s triad of biliary pain, jaundice, and fever. Acute cholangitis represents a medical emergency.
Acute pancreatitis: epigastric pain radiating to the back results from bile duct stones obstructing the pancreatic ducts. Inflammatory features include peritonitis.

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117
Q

Recognise the signs of gallstones and biliary colic on physical examination

A

Biliary colic: Right upper quadrant or epigastric tenderness.
Acute cholecystitis: Tachycardia, pyrexia, right upper quadrant or epigastric tenderness. There may be guarding +/- rebound. Murphy’s sign is elicited by placing a hand at the costal margin in the RUQ and asking the patient to breathe deeply. Patient stops breathing as the inflamed gallbladder descends and contacts the palpating fingers.
Ascending cholangitis: Pyrexia, right upper quadrant pain, jaundice.

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118
Q

Identify appropriate investigations for gallstones and biliary colic and interpret the results

A

Bloods: usually normal, LFTs can show raised bilirubin and AlkPhos
FBC, LFTs, serum lipase and amylase, abdominal ultrasound
MRCP, endoscopic ultrasound scan, ECRP, abdominal CT scan

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119
Q

Generate a management plan for gallstones and biliary colic

A

No treatment for asymptomatic cholecystolithiasis
symptomatic cholecystolithiasis: Laparoscopic cholecystectomy

cholelithiasis: ERCP, lithotripsy, papillary balloon dilation, stent

Relief of symptoms and electrolyte/fluid imbalance

  • Anti-emetics (dimenhydrinate)
  • Pain: NSAIDs (diclofenac)
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120
Q

Identify the possible complications of gallstones and biliary colic and its management

A

Cholecystitis, cholangitis, pancreatitis
Delayed surgery can cause pancreatitis, empyema/perforation of gallbladder, cholecystitis, cholangitis, obstructive jaundice

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121
Q

Summarise the prognosis for patients with gallstones and biliary colic

A

Good, dependant on development of complications
The outlook for patients with symptomatic cholelithiasis managed by cholecystectomy is favourable. The same holds for patients with choledocholithiasis who undergo ERCP with biliary sphincterotomy and stone extraction, followed later by cholecystectomy.

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122
Q

Define gastric cancer

A

Gastric malignancy, most commonly adenocarcinoma, more rarely lymphoma, leiomyosarcoma.
cancer deriving from the stomach

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123
Q

Explain the aetiology / risk factors of gastric cancer

A

50% involve pylorus
25% lesser curve
10% cardia
2-7% are lymphomas

Most cases are probably caused by environmental insults in genetically predisposed individuals that lead to mutation and subsequent unregulated cell growth.
Risk Factors: being >55, male, poor socio-economic status,
• H.pylori infection;
• atrophic gastritis;
• diet high in smoked, processed foods and nitrosamines; low vegetable consumption
• smoking
• alcohol

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124
Q

Summarise the epidemiology of gastric cancer

A

Common cause of cancer death worldwide, highest incidence in Asia (Japan). Sixth most common cancer in UK (annual incidence is 15 in 100000)
Age>50 years.

Cancer of the antrum/body is becoming less common, while that of the cardia and gastro- oesophageal junction is increasing.

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125
Q

Recognise the presenting symptoms of gastric cancer

A

In early phases, it is often asymptomatic. Early satiety or epigastric discomfort.
Weight loss, anorexia, nausea and vomiting.
dyspepsia
Haematemesis, melaena, symptoms of anaemia. Dysphagia (tumours of the cardia).
Symptoms of metastases, particularly abdominal swelling (ascites) or jaundice (liver involvement).

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126
Q

Recognise the signs of gastric cancer on physical examination

A

Physical examination may be normal.
Epigastric mass. Abdominal tenderness. Ascites. Hepatomegaly, jaundice, ascites
acanthosis nigricans
Signs of anaemia.
Many eponymous signs:
Virchow’s node/Troisier’s sign: Lymphadenopathy in left supraclavicular fossa.
Sister Mary Joseph node: Metastatic nodule on umbilicus.
Krukenberg’s tumour: Ovarian metastases.

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127
Q

Identify appropriate investigations for gastric cancer and interpret the results

A

Upper GI endoscopy: With multiquadrant biopsy of all gastric ulcers.
Blood: FBC (for anaemia), LFT. CEA, Ca19-9, Ca72-4
CT/MRI: Staging of tumour and planning of surgery.
Ultrasound of liver: Staging of tumour.
Bone scan: Staging of tumour.
Endoscopic ultrasound: Assesses depth of invasion and lymph node spread.
Laparoscopy: May be needed to determine if tumour is resectable.

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128
Q

Define gastro-oesophageal reflux disease

A

Inflammation of the oesophagus caused by reflux of gastric acid and/or bile

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129
Q

Explain the aetiology / risk factors of gastro-oesophageal reflux disease

A

Disruptions of mechanisms that prevent reflux (physiological etc.)
Risk Factors: obesity, pregnancy (increase in abdominal pressure), smoking, diet, hiatus hernia, increase in age, FHx

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130
Q

Summarise the epidemiology of gastro-oesophageal reflux disease

A

Common, 5-10% of adults

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131
Q

Recognise the presenting symptoms of gastro-oesophageal reflux disease

A

Substernal burning discomfort or ‘heartburn’, aggravated by supine position, bending, large meals and drinking alcohol
acid regurgitation
Waterbrash
Aspiration results in voice hoarseness, laryngitis, nocturnal cough and wheeze
dysphagia, bloating, early satiety

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132
Q

Recognise the signs of gastro-oesophageal reflux disease on physical examination

A

Usually normal.

Occasionally, epigastric tenderness, wheeze on chest auscultation, dysphonia.

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133
Q

Identify appropriate investigations for gastro-oesophageal reflux disease and interpret the results

A

Upper GI Endoscopy, biopsy: confirm presence of oesophagitis, exclude malignancy
Barium Swallow: detect hiatus hernia, peptic stricture

CXR: incidental hiatus hernia findings
24 hour oesophageal pH monitoring: determines temporal relationship to symptoms

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134
Q

Generate a management plan for gastro-oesophageal reflux disease

A

Advice:
- Lifestyle changes, weight loss, elevating head
- Avoid provoking factors, stopping smoking, lower fat meals
Medical:
- Antacids
- PPIs (e.g. lansoprazole)
- H2 antagonists (e.g. ranitidine)
Endoscopy:
- Annual endoscopic surveillance for Barrett’s Oesophagus Surgery:
- Anti-reflux surgery

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135
Q

Identify the possible complications of gastro-oesophageal reflux disease and its management

A

Oesophageal ulceration; peptic stricture; anaemia; Barrett’s; oesophageal adenocarcinoma

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136
Q

Summarise the prognosis for patients with gastro-oesophageal reflux disease

A

50% respond to lifestyle changes alone

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137
Q

Define gastroenteritis

A

Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort

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138
Q

Explain the aetiology / risk factors of gastroenteritis & infectious colitis

i.e. name some of the pathogens

A 
Viral:
- Rotavirus, astrovirus, calcivirus
Bacterial:
- Campylobacter jejuni, Escherichia coli, Salmonella, Shigella
Protozoal:
- Entamoeba histolytica
Toxins:
- From Staphylococcus aureus, Clostridium botulinum

Commonly contaminated foods: improperly cooked meats, old rice, eggs, poultry

CHESS organisms

  • Campylobacter
  • Haemorrhagic E. Coli
  • Entamoeba histolytica
  • Shigella
  • Salmonella
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139
Q

Summarise the epidemiology of gastroenteritis

A

Common, often under-reported

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140
Q

Recognise the presenting symptoms of gastroenteritis

A

Sudden onset nausea, vomiting, anorexia
Diarrhoea, abdominal pain/discomfort, fever, malaise

Enquire: recent travel, antibiotic use and recent food intake
Time: toxins (1-24 hours), bacterial (12 hours)

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141
Q

Recognise the signs of gastroenteritis (&IC)

A

Diffuse abdominal tenderness, abdominal distension and bowel sounds are increased
Severe: pyrexia, dehydration, hypotension, peripheral shutdown

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142
Q

Identify appropriate investigations for gastroenteritis & infectious colitis and interpret the results

A

Bloods: FBC, culture, U&Es
Stool: faecal microscopy
AXR/USS: exclude other causes
Sigmoidoscopy: only if IBD needs to be excluded

INFECTIOUS COLITIS
Bloods: FBC, CRP, ESR
Stool: MC&S

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143
Q

Generate a management plan for gastroenteritis & infectious colitis

A

Bed rest, fluids and electrolyte replacement (advise increase oral fluid intake to compensate for the water lost from diarrhoea and vomiting)
IV rehydration may be required in severe cases. Don;’t conventionally give antibiotics unless a bacteria has been isolated.
Botulism: botulinum antitoxin IM, manage in ITU

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144
Q

Identify the possible complications of gastroenteritis & infectious colitis and its management

A

Dehydration, electrolyte imbalance, prerenal failure, sepsis, shock
Botulinum: respiratory muscle paralysis

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145
Q

Summarise the prognosis for patients with gastroenteritis & infectious colitis

A

Generally good, majority are self-limiting

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146
Q

Define infectious colitis

A

An inflammation of the large bowel, with an infective cause

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147
Q

Summarise the epidemiology of infectious colitis

A

Rare, in those with lower hygiene levels, and contaminated food

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148
Q

Recognise the presenting symptoms of infectious colitis

A

Bloody diarrhoea, generalised abdominal pain, vomiting

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149
Q

Recognise the signs of infectious colitis on physical examination

A

Tenderness

DRE: bloody stool

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150
Q

Define gastrointestinal perforation

A

A hole in the wall of the gastrointestinal tract

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151
Q

Explain the aetiology / risk factors of gastrointestinal perforation

A

Gastric ulcers, duodenal ulcers, appendicitis, gastrointestinal cancer, diverticulitis
Iatrogenic: abdominal surgery

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152
Q

Summarise the epidemiology of gastrointestinal perforation

A

10-15% of patients with acute diverticulitis

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153
Q

Recognise the presenting symptoms of gastrointestinal perforation

A

Sudden pain in epigastrium (duodenal ulcer), burning pain in epigastrium (gastric ulcer) Pain starts at perforation site, then spreads
Severe abdominal pain, nausea, vomiting and hematemesis

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154
Q

Recognise the signs of gastrointestinal perforation on physical examination

A

Severe abdominal tenderness and rigidity

Fever, silent bowel sounds, distended abdomen, tachycardia, dyspnoea

155
Q

Identify appropriate investigations for gastrointestinal perforation and interpret the results

A

Bloods: FBC, CRP, ESR, U&Es, LFTs
AXR: gas under diaphragm
CT Abdomen: may visualise location of perforation

156
Q

Generate a management plan for gastrointestinal perforation

A 
Surgical Intervention: peritoneal wash and anatomical repair
Conservative:
- IV fluids
- Antibiotics
- Nasogastric aspiration and bowel rest
157
Q

Identify the possible complications of gastrointestinal perforation and its management

A

Peritonitis, bleeding, bowel infarction, sepsis, shock

158
Q

Summarise the prognosis for patients with gastrointestinal perforation

A

Depends on size and location; worse prognosis in older patients with existing bowel disease

159
Q

Define haemochromatosis

A

Deficiency of hepcidin, resulting in an accumulation of iron

160
Q

Explain the aetiology / risk factors of haemochromatosis

A

Defects of the HFE gene

161
Q

Summarise the epidemiology of haemochromatosis

162
Q

Recognise the presenting symptoms of haemochromatosis

A

Early: vague and nonspecific (fatigue, weakness)
Late: diabetes, bronzing of the skin, impaired memory, depression

163
Q

Recognise the signs of haemochromatosis on physical examination

A

Hepatomegaly, diabetes mellitus, arrhythmias,

164
Q

Identify appropriate investigations for haemochromatosis and interpret the results

A

Bloods: serum iron, serum ferritin, transferrin saturation, LFTs Genetic testing: HFE testing
Liver biopsy: rarely required

165
Q

Define haemorrhoids

A

Abnormally enlarged vascular mucosal cushions in the anal canal.
They are either internal (above the dentate line) or external (below the dentate line)

Internal Haemorrhoids: classified according to the degree of prolapse
- First Degree: do not prolapse
- Second Degree: prolapse on straining, reduce spontaneously
- Third Degree: prolapse on straining, can be reduced manually
- Fourth Degree: permanently prolapsed, cannot be reduced
They are painless unless strangulated

External Haemorrhoids

  • Can be painful and itchy
  • May be visible on external examination
166
Q

Explain the aetiology / risk factors of haemorrhoids

A

Caused by excessive straining due to either chronic constipation or diarrhoea. Repetitive or prolonged straining causes downward stress on the vascular haemorrhoidal cushions, leading to the disruption of the supporting tissue elements with subsequent elongation, dilation, and engorgement of the haemorrhoidal tissues.Other conditions can contribute to the formation of haemorrhoids: an increase in intra-abdominal pressure in pregnancy or ascites.

Risk Factors: constipation, prolonged straining, increased abdominal pressure (pregnancy, ascites, childbirth), heavy lifting, chronic cough

167
Q

Summarise the epidemiology of haemorrhoids

A

13-36% of population

168
Q

Recognise the presenting symptoms of haemorrhoids

A

May be asymptomatic
Bright red, painless rectal bleeding with defecation, not mixed with stool.
Anal itching or irritation
Feeling of rectal fullness, discomfort or incomplete evacuation
Strangulated: intensely painful

169
Q

Recognise the signs of haemorrhoids on physical examination

A

Non-prolapsed haemorrhoids are not evident on external examination, difficult to feel in DRE
Local perianal irritation can be seen in chronic discharge
Asking patient to strain can make haemorrhoids visible
Thrombosed: purple, swollen, acutely tender, perianal lumps

170
Q

Identify appropriate investigations for haemorrhoids and interpret the results

A

Bloods: FBC, CRP
Proctoscopy: should be carried out to aid diagnosis
Flexible sigmoidoscopy/colonoscopy: exclude other pathology

171
Q

Generate a management plan for haemorrhoids

A

Depends on degree of prolapse
Prevention and management of constipation:
- Fluids and fibre intake
Pain and symptom relief:
- Simple analgesia e.g. paracetamol
- Topical therapies: topical anaesthetics or corticosteroids Non-Surgical:
- Rubber band ligation: band cuts off blood supply, necrotising the haemorrhoid and it falls off
- Good for Grade II haemorrhoids
Surgical:
- Haemorrhoidectomy: painful, performed under GA Thrombosed Haemorrhoids:
- Extremely painful, treat conservatively with analgesia

172
Q

Identify the possible complications of haemorrhoids and its management

A

Skin tags, ischaemia, perianal sepsis, thrombosed haemorrhoids can ulcerate

173
Q

Summarise the prognosis for patients with haemorrhoids

A

Generally good, 10% may need surgery

174
Q

Define hepatocellular carcinoma

A

Primary malignancy of hepatocytes, usually occurring in a cirrhotic liver. Mostly occurs in those with chronic liver disease
cancer of the hepatocytes

175
Q

Explain the aetiology / risk factors of hepatocellular carcinoma

A
  • Chronic liver damage (e.g. alcoholic liver disease, hepatitis B, hepatitis C, autoimmune disease, primary biliary cirrhosis),
  • metabolic disease (e.g. haemochromatosis), and
  • aflatoxins (Aspergillus flavus fungal toxin found on stored grains or biological weapons).
176
Q

Summarise the epidemiology of hepatocellular carcinoma

A

common makes up 1-2% of malignancies
very common malignancy in areas where Hepatitis B and C are endemic, i.e. Asia and sub-Saharan Africa ( 500 in 100,000/year). Not common in the west.

177
Q

Recognise the presenting symptoms of hepatocellular carcinoma

A

Symptoms of malignancy: Malaise, weight loss, loss of appetite.
Symptoms of chronic liver disease: Abdominal distension, jaundice, RUQ pain. Pruritus, bleeding oesophageal varices
History of carcinogen exposure: High alcohol intake, Hepatitis B or C, aflatoxins.

178
Q

Recognise the signs of hepatocellular carcinoma on physical examination

A

Signs of malignancy: Cachexia/weight loss, lymphadenopathy.
Hepatomegaly: Nodular (but may be smooth). Deep palpation may elicit tenderness. There may be bruit heard over the liver.
Signs of chronic liver disease: Jaundice, ascites, RUQ pain, confusion (see Cirrhosis).

179
Q

Identify appropriate investigations for hepatocellular carcinoma and interpret the results

A

Bloods: FBC, LFTs, clotting, alpha fetoprotein, AFP
CT/MRI: imaging and staging
Biopsy: cytology

180
Q

Define hernias (femoral)

A 
A herniation of the contents of the abdomen through the femoral canal
Femoral canal:
- Anterior border: inguinal ligament
- Posterior border: pectineal ligament
- Medial border: lacunar ligament
- Lateral border: femoral vein
181
Q

Explain the aetiology / risk factors of hernias (femoral, inguinal, miscellaneous)

A

Weakening of abdominal wall allows hernias to protrude through in an increase of intra-abdominal pressure

RF: old age, smoking, FHx, gender (female=femoral, male=inguinal), prematurity, pregnancy, weight lifting, constipation, weight gain, chronic cough and previous abdominal surgery/trauma

182
Q

Summarise the epidemiology of hernias (femoral)

A

Account for 5% of abdominal hernias

183
Q

Recognise the presenting symptoms of hernias (femoral)

A

Femoral:
- Lump in groin, lateral and inferior to pubic tubercle
- Appears/swells on coughing, and reduces on relaxation or supination
- May be possible to reduce hernia
Strangulated: tender, colicky abdominal pain, distension, vomiting

184
Q

Recognise the signs of hernias (femoral) on physical examination

A

Hernias: reducible, irreducible, obstructed or strangulated Strangulated: lump becomes red and tender

185
Q

Identify appropriate investigations for hernias (femoral, inguinal, miscellaneous) and interpret the results

A

Diagnosis is largely clinical

Imaging: USS is first line, followed by CT/MRI

186
Q

Generate a management plan for hernias (femoral)

A

Surgical repair in elective surgery: dissection of the sac, reduction of its contents, completed with sac ligation

187
Q

Identify the possible complications of hernias (femoral) and its management

A

risk of strangulation at 22%

188
Q

Summarise the prognosis for patients with hernias (femoral, inguinal, miscellaneous)

A

Good prognosis, mortality for strangulated hernias lies at 2-13%

189
Q

Generate a management plan for hernias (inguinal)

A
  • If small, may only need reassurance

- Elective surgery: dissection of sac, reduction of contents, ligation of sac

190
Q

Identify the possible complications of hernias (inguinal) and its management

A

recurrence, wound infection, bladder injury, intestinal injury

191
Q

Define hiatus hernias

A

A herniation of part of the abdominal contents through the oesophageal aperture of the diaphragm
Sliding (90%):Gastro-oesophageal junction slides up in to thoracic cavity
Rolling (10%): Gastro-oesophageal junction remains in place but a part of the stomach herniates into chest

192
Q

Explain the aetiology / risk factors of hiatus hernias

A

One or more of three mechanisms:

  • Widening of diaphragmatic hiatus
  • Pulling up of the stomach due to oesophageal shortening
  • Pushing up of the stomach by increased intra-abdominal pressure

Risk Factors: increased abdominal pressure (obesity, pregnancy, ascites), age, previous hiatus operation.

193
Q

Recognise the presenting symptoms of hiatus hernias

A

Sliding:
- Can be asymptomatic, retrosternal burning/heartburn, GORD, dysphagia
Rolling:
- Can be asymptomatic, chest pain, epigastric pain or fullness, nausea

May be asymptomatic or may present with heartburn, dysphagia, odynophagia, hoarseness, asthma, shortness of breath, chest pain, anaemia or haematemesis, or some combination of these.

194
Q

Recognise the signs of hiatus hernias on physical examination

A

See symptoms: tender abdomen

195
Q

Identify appropriate investigations for hiatus hernias and interpret the results

A

Contrasted upper gastrointestinal series (also known as an upper GI or as a barium oesophagram) is the key investigation.
CXR
endoscopy

196
Q

Generate a management plan for hiatus hernias

A

Lifestyle: avoid factors that increase intra-abdominal pressure Pharmacological: PPIs, H2 receptor antagonists
Surgical: not asymptomatic sliding hernias, laparoscopic fundoplication

Uncomplicated sliding hiatus hernias are treated symptomatically with medical therapy, although some patients may select surgical therapy. Complicated hiatus hernias (those with bleeding, volvulus, or obstruction) have a stronger indication for surgical repair.

197
Q

Identify the possible complications of hiatus hernias and its management

A

obstruction, bleeding, volvulus with and without strangulation or necrosis, and Barrett’s oesophagus

Side effects of bloating and dysphagia, recurrence

198
Q

Summarise the prognosis for patients with hiatus hernias

A

Gain symptomatic relief with medical/surgical treatment, morbidity and mortality higher in >70

199
Q

Define intestinal ischaemia

A

Impaired blood transfusion to the intestine, resulting in ischaemia of the bowel wall

200
Q

Summarise the epidemiology of intestinal ischaemia

A

Mainly >50

201
Q

Recognise the signs of intestinal ischaemia on physical examination

A

tenderness and rebound

cachexia

202
Q

Explain the aetiology / risk factors of intestinal ischaemia

A

Conditions causing arterial emboli or thrombosis

Risk Factors: 
• old age
• history of smoking
• hypercoagulable states
• atrial fibrillation
203
Q

Recognise the presenting symptoms of intestinal ischaemia

A

sudden severe pain, N&V

Colicky/constant and poorly localised abdominal pain

204
Q

Identify appropriate investigations for intestinal ischaemia and interpret the results

A

AXR: rule out other causes
Angiography: to show blockage
ECG: leucocytosis and possible anaemia (if bleeding)

205
Q

Define intestinal obstruction

A

Mechanical obstruction of the bowel lumen (extrinsic or intrinsic) causing blockage of the intestines

206
Q

Explain the aetiology / risk factors of intestinal obstruction

A 
Small Bowel:
- Adhesions from prior operations
- Malignancy
Large Bowel:
- Colorectal malignancies
Sigmoid/caecal volvulus
Paralytic Ileus
Postoperative ileus

Risk factors
• previous abdominal surgery
• malrotation
• Crohn's disease
•  hernia
207
Q

Summarise the epidemiology of intestinal obstruction

A

Most are small bowel

208
Q

Recognise the presenting symptoms of intestinal obstruction

A 
Diffuse, central colicky pain
Vomiting (higher obstruction)
[Progression is faster in small bowel]
Abdominal distension
Progressive constipation and bloating
failure to pass flatus or stool
209
Q

Recognise the signs of intestinal obstruction on physical examination

A

Abdominal distension, tympany, high pitched, tinkling bowel sounds
Pyrexia – suggests perforation or infarction of bowel

210
Q

Identify appropriate investigations for intestinal obstruction and interpret the results

A

Bloods: FBC, U&Es, creatinine, group and save
Fluid charts
Plain AXR & CT

211
Q

Generate a management plan for intestinal obstruction

A 
Surgery:
- Laparotomy, if no clear diagnosis
- Required if signs of peritonitis
Non-Surgical treatment:
- Drip and suck (bowel decompression)
Volvulus:
- Can be treated conservatively unless decompression fails/perforation
212
Q

Identify the possible complications of intestinal obstruction and its management

A

Any carcinoma causing obstruction is already advanced

Perforation can cause peritonitis and ischaemia

213
Q

Summarise the prognosis for patients with intestinal obstruction

A

Small bowel: mortality at 25% with delayed surgery >36 hours; drops to 8% at <36 hours

214
Q

What is functional dyspepsia?

A

also known as non-ulcer dyspepsia or indigestion, is a term used to describe a group of symptoms affecting the GI tract, including stomach pain or discomfort, nausea, bloating and belching

characterised by troublesome early satiety, fullness, or epigastric pain or burning. It can be overlooked as the symptoms overlap with GORD and IBS

a chronic disorder of sensation and movement (peristalsis) in the upper GI tract. The cause is unknown; however, several hypotheses could explain this condition. Excessive acid secretion, inflammation of the stomach or duodenum, food allergies, lifestyle and diet influences, psychological factors, medication side effects (from NSAIDs and aspirin), and H.pylori infection have all had their proponents.

215
Q

Define irritable bowel syndrome (IBS)

A

A functional bowel disorder defined as recurrent episodes of abdominal pain and discomfort for >6 months, associated with >2 of the following:

  • Altered stool passage
  • Abdominal bloating
  • Worsening on eating
  • Passage of mucous
216
Q

Explain the aetiology / risk factors of functional dyspepsia & irritable bowel syndrome (IBS)

A

Unknown, psychological factors

217
Q

Summarise the epidemiology of irritable bowel syndrome (IBS)

A

Common, 10-20% of adults, females 2x more than men

218
Q

Recognise the presenting symptoms of functional dyspepsia & irritable bowel syndrome (IBS)

A

> 6 month history of abdominal pain (colicky in lower abdomen, relieved with defecation/flatus)
3 bowel motions daily or <3 a week
Abdominal bloating, change in stool consistency - diarrhoea and constipation

Screen for ‘red flag’: weight loss, anaemia, PR bleeding, late onset (>60 years)

219
Q

Recognise the signs of irritable bowel syndrome (IBS) on physical examination

A

Normally absent signs on examination – can be distended and mildly tender in iliac fossae

220
Q

Identify appropriate investigations for irritable bowel syndrome (IBS) and interpret the results

A

Diagnosis made by history, investigations used to exclude pathology Bloods: FBC, LFTs, ESR, CRP, TFT
Stool examination: MC&S
USS: excludes gallstones
Hydrogen Breath Test: exclusion of H pylori infection

221
Q

Generate a management plan for irritable bowel syndrome (IBS)

A 
Advice:
- Dietary modification
Medical:
- Antispasmodics e.g. buscopan
- Prokinetic agents e.g. metoclopramide
- Antidiarrhoeals e.g. loperamide
- Laxatives e.g. lactulose
- Tricyclic antidepressants
Psychological Therapies
- CBT/relaxation for stress
222
Q

Identify the possible complications of irritable bowel syndrome (IBS) and its management

A

Increase risk of colonic diverticulosis

223
Q

Summarise the prognosis for patients with irritable bowel syndrome (IBS)

A

Chronic, and relapsing condition – can be exacerbated by stress

224
Q

Define liver abscesses

A

Abscesses found on the liver (localised infection of liver parenchyma)

225
Q

Summarise the epidemiology of liver abscesses

A

Caused by bacterial, parasitic or fungal organisms

226
Q

Recognise the presenting symptoms of liver abscesses

A

Multiple abscesses tend to present more acutely

RUQ pain, tenderness, night sweats, nausea and vomiting, anorexia, dyspnoea

227
Q

Recognise the signs of liver abscesses on physical examination

A

Hepatomegaly, jaundice, pyrexia

228
Q

Identify appropriate investigations for liver abscesses and interpret the results

A

Bloods: FBC, ESR, CRP, LFTs
USS: shows abscess

229
Q

Explain the aetiology / risk factors of liver cysts

A

Thought to be congenital

230
Q

Recognise the presenting symptoms of liver cysts

A

Usually asymptomatic,

Can cause RUQ pain and bloating symptoms

231
Q

Recognise the signs of liver cysts on physical examination

A

Jaundice, RUQ tenderness

232
Q

Identify appropriate investigations for liver cysts and interpret the results

A

Bloods: FBC, LFTs
Imaging: USS/CT/MRI to show cyst anatomy

233
Q

Summarise the epidemiology of liver cysts

A

11% incidence

234
Q

Define liver failure

A

Severe liver dysfunction, causing jaundice, encephalopathy and coagulopathy
Hyperacute: <7 days
Acute: 1-4 weeks
Sub-acute: 4-12 weeks
Acute-on-chronic: acute deterioration in chronic liver disease patients

235
Q

Explain the aetiology / risk factors of liver failure

A

Drugs: paracetamol
Viral: Hep A/B/D/E
Other: autoimmune liver failure; Budd-Chiari syndrome Pathogenesis:
- Jaundice: decreased conjugated bilirubin
- Encephalopathy: increased delivery of gut products to systemic circulation
- Coagulopathy: decreased clotting factor synthesis

Risk Factors
	• chronic alcohol abuse
	• poor nutritional status
	• female sex
	• age >40 years
236
Q

Summarise the epidemiology of liver failure

A

Paracetamol overdose accounts for 50% of all liver failures

237
Q

Recognise the presenting symptoms of liver failure

A

Can be asymptomatic
Fever, nausea, jaundice
abdominal pain, nausea and vomiting

238
Q

Recognise the signs of liver failure on physical examination

A

Jaundice, encephalopathy, liver asterixis, fetor hepaticus Ascites and splenomegaly, bruising, bleeding
Pyrexia

239
Q

Identify appropriate investigations for liver failure and interpret the results

A

Identify Cause:
- Viral serology, paracetamol levels, autoantibodies
Bloods: FBC, LFTs, U&Es, glucose, coagulation, ABG, group and save USS/CT: image liver
Ascitic fluid: MC&S
Doppler: exclude Budd-Chiari syndrome

240
Q

Generate a management plan for liver failure

A

Resuscitation: ABC
Treat Cause: paracetamol overdose Treat/Prevent Complications:
- Monitor: vital signs
- Manage encephalopathy: lactulose
- Antibiotic and antifungal prophylaxis
- Hypoglycaemia treatment
- Coagulopathy treatment: IV Vitamin K
- Gastric mucosa protection: PPI
- Avoid: sedatives or liver metabolised drugs
- Cerebral Oedema: decrease ICP using mannitol

241
Q

Identify the possible complications of liver failure and its management

A

Infection, coagulopathy, hypoglycaemia, cerebral oedema, raised ICP

242
Q

Summarise the prognosis for patients with liver failure

A

Depends on severity

243
Q

Define Mallory-Weiss tear

A

Mucosal lacerations in the upper gastrointestinal tract; usually at gastro-oesophageal junction or gastric cardia

244
Q

Explain the aetiology / risk factors of a Mallory-Weiss tear

A

Can be caused by a sudden increase in intragastric pressure

Risk factors: excess alcohol, hyperemesis gravidarum, bulimia, hepatitis, chronic cough

245
Q

Summarise the epidemiology of a Mallory-Weiss tear

A

Account for 4-8% of upper GI bleeds

246
Q

Recognise the presenting symptoms of a Mallory-Weiss tear

A

Haematemesis, following a bout of retching or vomiting

Melaena, light-headedness, dizziness, syncope

247
Q

Recognise the signs of a Mallory-Weiss tear on physical examination

A

Bloods: FBC, clotting screening, U&Es, creatinine, group & save, cardiac enzymes
ECG

248
Q

Identify the possible complications of a Mallory-Weiss tear and its management

A

Vomiting: electrolyte imbalances
Bleeding: hypovolaemic shock and death
Comorbidities: MI, hepatitis

249
Q

Summarise the prognosis for patients with a Mallory-Weiss tear

A

Prognosis usually excellent, tears heal rapidly within 48-72 hours; re-bleeding in 8-20% of cases

250
Q

Define NASH

A

non-alcoholic steatohepatitis

251
Q

Define NASH

A

non-alcoholic steatohepatitis - An accumulation of fat in the liver, associated with inflammation, not due to excessive alcohol intake

252
Q

Explain the aetiology / risk factors of non-alcoholic steatohepatitis (NASH)

A

An accumulation of triglycerides and other lipids within hepatocytes
Risk Factors: T2DM, polycystuc ovary syndrome, HepB/C HIV, Drugs (amiodarone, tamoxifen), metabolic disorders (Wilson’s)

253
Q

Summarise the epidemiology of non-alcoholic steatohepatitis (NASH)

A

Most common cause of deranged LFTs

254
Q

Recognise the presenting symptoms of non-alcoholic steatohepatitis (NASH)

A

Most are asymptomatic – but may report fatigue, malaise or RUQ pain
Can present with symptoms of cirrhosis (ascites, oedema and jaundice)

255
Q

Recognise the signs of non-alcoholic steatohepatitis (NASH) on physical examination

A

Hepatomegaly, splenomegaly, signs of chronic liver disease (spider naevi, ascites, oedema, ABCDE)

256
Q

Identify appropriate investigations for non-alcoholic steatohepatitis (NASH) and interpret the results

A

Definitive diagnosis can only be made with biopsy
Bloods: LFTs, FBC, lipids
Imaging: USS/CT
Biopsy: only way to diagnose

257
Q

Generate a management plan for non-alcoholic steatohepatitis (NASH)

A

Advice:
• Adequate diet
• Weight loss, and control of comorbidities

258
Q

Identify the possible complications of non-alcoholic steatohepatitis (NASH) and its management

A

Can progress to cirrhosis and liver failure

259
Q

Summarise the prognosis for patients with non-alcoholic steatohepatitis (NASH)

A

Depends on the stage of disease

260
Q

Define oesophageal cancer

A

Cancer derived from oesophageal cells

261
Q

Explain the aetiology / risk factors of oesophageal cancer

A

Majority are SCC and adenocarcinomas
Risk Factors: smoking, alcohol, Caucasian, Barrett’s Oesophagus

UK: usually adenocarcinoma (as a result of Barrett’s oesophagus)
Smoking, some Mediterranean/Chinese foods: squamous cell carcinoma

262
Q

Summarise the epidemiology of oesophageal cancer

A

Common, aggressive tumour

263
Q

Recognise the presenting symptoms of oesophageal cancer

A

Dysphagia, vomiting, anorexia and weight loss, symptoms of GI blood loss

264
Q

Recognise the signs of oesophageal cancer on physical examination

A

Lymphadenopathy, weight loss

265
Q

Recognise the signs of oesophageal cancer on physical examination

A

Lymphadenopathy, weight loss

266
Q

Identify appropriate investigations for oesophageal cancer and interpret the results

A

Bloods: CEA, Ca19-9, FBC, U&Es, LFTs, glucose, CRP
Endoscopy: with biopsy of any lesions
CXR: metastases

267
Q

Define pancreatic cancer

A

Cancer deriving from pancreatic tissue

268
Q

Explain the aetiology / risk factors of pancreatic cancer

A

11th most common cancer, 5th most common cause of cancer death

269
Q

Summarise the epidemiology of pancreatic cancer

A

Risk Factors: smoking, diet (high BMI, read meat, low vegetables), diabetes, alcohol

270
Q

Recognise the presenting symptoms of pancreatic cancer

A

Presents quite late
Progressive painless jaundice
Late symptoms: abdominal pain, acute pancreatitis, weight loss, haematemesis

271
Q

Recognise the signs of pancreatic cancer on physical examination

A

Courvoisier’s sign, abdominal tenderness, jaundice

272
Q

Identify appropriate investigations for pancreatic cancer and interpret the results

A

Bloods: Ca19-9, FBC, LFTs, glucose
Imaging: USS, abdominal CT, Endoscopic ultrasound

273
Q

What is Courvoisier’s sign?

A

gallbladder that’s enlarged due to bile buildup (can usually see or feel it)
no pain
jaundice
not caused by a gallbladder stone, usually a tumour

‘in the presence of a palpably enlarged gallbladder which is non-tender and accompanied with mild painless jaundice, the cause is unlikely to be gallstones.’

274
Q

Define acute pancreatitis

A

autodigestion of the pancreatic tissue

275
Q

Explain the aetiology / risk factors of acute pancreatitis

A

caused by alcohol abuse and gallstones

276
Q

Explain the aetiology / risk factors of acute pancreatitis

A

caused by alcohol abuse and gallstones

277
Q

Summarise the epidemiology of acute pancreatitis

A

common, but usually not severe

278
Q

Recognise the signs of acute pancreatitis on physical examination

A

cullens and grey-turners
mass
tender epigastric region

279
Q

Recognise the signs of acute pancreatitis on physical examination

A

cullens and grey-turners
mass
tender epigastric region

280
Q

Identify appropriate investigations for acute pancreatitis and interpret the results

A

bloods: hypocalcaemia (fat necrosis), FBC, CRP,

281
Q

Generate a management plan for acute pancreatitis

A
  • initial fluid resuscitation (+ oxygen. analgesia and anti-emesis if necessary)
  • Choledocholithiasis without cholangitis - cholecystectomy
    Cholecystectomy should be delayed in patients with severe/necrotising acute pancreatitis.
  • gallstone pancreatitis with cholangitis - ERCP within 24 hours
  • Alcohol-induced pancreatitis: counselling intervention during admission. may need pharmacological treatment for alcohol withdrawal. Vitamin, thiamine and folic acid replacement
  • with infected pancreatic necrosis: IV ABs, catheter and surgery?
282
Q

Identify the possible complications of acute pancreatitis and its management

A

Local: pancreatic necrosis, pseudocyst
Systemic: MODS, sepsis, renal failure, ARDS
Long Term: chronic pancreatitis

283
Q

Summarise the prognosis for patients with acute pancreatitis

A

20% run severe course with 70% mortality, 80% run milder with 5% mortality

284
Q

Define chronic pancreatitis

A

Chronic pancreatitisis inflammation due to irreversible changes to the pancreatic structure, likefibrosis, atrophy and calcification.
Healthy tissue is replaced by misshaped/stenosed ducts (caused by fibrosis of the ducts), (acinar) atrophy and calcification. This leads to adrenal insufficiency.

Chronic inflammatory disease of the pancreas resulting in irreversible parenchymal atrophy and fibrosis, causing, in turn, impaired endocrine and exocrine function and recurrent abdominal pain

285
Q

Explain the aetiology / risk factors of acute pancreatitis

A

Severe epigastric pain, radiating to the back, relieved by sitting forward
Aggravated by movement, exacerbated by eating or drinking alcohol.
Weight loss, bloating and steatorrhea
Associated with anorexia, nausea and vomiting
IMPORTANT: check whether the patient has a history of high alcohol intake or gallstones

286
Q

Recognise the signs of acute pancreatitis on physical examination

A

Epigastric tenderness
Fever
Shock (includes tachycardia and tachypnoea)
Decreased bowel sounds (due to ileus)
In severe pancreatitis:
- Cullen’s sign (periumbilical bruising)
- Grey-Turner sign (flank bruising)

287
Q

Identify appropriate investigations for acute pancreatitis and interpret the results

A

Bloods: glucose, amylase, lipase, hypocalcaemia, CRP
ERCP/MRCP: early changes are duct dilatation and stumping of branches; late changes are duct strictures with alternating dilatation
AXR: pancreatic calcification

288
Q

Generate a management plan for acute pancreatitis

A

General:
- Mainly symptomatic treatment and supportive
Endoscopic therapy:
- Sphincterotomy, stone extraction
- Extracorporeal shock-wave lithotripsy used for fragmentation prior to endoscopic removal
Surgical:
- Indicated if conservative management failed

289
Q

Identify the possible complications of acute pancreatitis and its management

A

Local:
- Pseudocysts, duodenal obstruction, pancreatic ascites
Systemic:
- Diabetes, steatorrhea, reduced quality of life

290
Q

Summarise the prognosis for patients with acute pancreatitis

A

Difficult to predict, life expectancy reduced by 10-20 years

291
Q

Define peptic ulcer disease and gastritis

A

Ulcerations in the GI tract caused by exposure to gastric acid and pepsin.

292
Q

Explain the aetiology / risk factors of peptic ulcer disease and gastritis

A

Imbalance of damaging pepsin and gastric acid with protective mucosal mechanisms.
Common: Very strong association with H pylori (95% of duodenal, 80% of gastric), NSAID use
Rare: Zollinger-Ellison syndrome: gastrin secreting pancreatic tumour

RF: H.pylori, smoking (increases acid production), age, NSAIDs, burns and head trauma can increase ulcer development

Pain- caused by breakdown reaches nerves
Bleeding- breakdown reaches blood vessels

293
Q

Summarise the epidemiology of peptic ulcer disease and gastritis

A

Common, more in men, and annual incidence of 1-4:1000, with duodenal ulcers being more common in younger people
Duodenal ulcers are 4x more common than gastric

294
Q

Recognise the presenting symptoms of peptic ulcer disease and gastritis

A

Epigastric pain, which is relieved by antacids
Variable relationship to food:
- If worse straight after eating, gastric
- If worse hours later/relieved after eating or drinking milk, duodenal
May have melaena and haematemesis
May have weight loss, but more common in gastric ulcers.
Pointing signs: they can point to where the pain is localised

H.pylori: epigastric pain that worsens with eating, postprandial belching and epigastric fullness, early satiety, fatty food intolerance, nausea, and occasional vomiting

295
Q

Recognise the signs of peptic ulcer disease and gastritis on physical examination

A

May be no physical findings

Epigastric tenderness and signs of complications

296
Q

Identify appropriate investigations for peptic ulcer disease and gastritis and interpret the results

A

Bloods: FBC, amylase, U&Es, clotting, LFT, cross-match, Secretin test (ZE)
Endoscopy: (over 55, or alarm symptoms) four quadrant ulcer biopsies to rule out malignancy, no need to biopsy duodenal ulcers
Rockall Scoring: for severity after GI bleed
H Pylori testing: (If under 55, with no alarm symptoms)
- C13-urea breath test
- Serology
- Stool antigen testing

297
Q

Generate a management plan for peptic ulcer disease and gastritis

A

Acute:
- Resuscitation if perforated/bleeding
- IV PPI (omeprazole)
Endoscopy:
- Haemostasis by electrocoagulation, laser
Surgery:
- If perforated or bleeding uncontrolled
H pylori Eradication:
- Tripe Therapy (clarithromycin, amoxicillin + PPI) for 1-2 weeks
If non-H pylori:
- Treat with PPIs or H2 antagonists, stop NSAID use

298
Q

Identify the possible complications of peptic ulcer disease and gastritis and its management

A

Haemorrhage, perforation

299
Q

Summarise the prognosis for patients with peptic ulcer disease and gastritis

A

Lifetime risk is 10%, usually good as can be cured with H pylori eradication

300
Q

Define perineal abscesses

A

Collection of pus in the anal/rectal region

301
Q

Define perineal fistulae

A

an abnormal chronically infected tract communicating between the perineal skin and either the anal canal or the rectum

302
Q

Explain the aetiology / risk factors of perineal abscesses and fistulae

A

Caused by bacterial infection of anal fissure, STIs or blocked anal glands
Fistulae develop as a complication of an abscess
Fistulae can develop as a complications of Crohn’s disease

Risk Factors:
IBD
Diabetes mellitus
Malignancy

303
Q

Summarise the epidemiology of perineal abscesses and fistulae

A

High risk groups include diabetes, immunocompromised, anal sex

common

304
Q

Recognise the presenting symptoms of perineal abscesses and fistulae

A

Painful hardened tissue in perianal area, constant throbbing pain in the perineum
Discharge of pus, lump/nodule, tenderness at anus edge, fever, constipation
Personal or family history of IBD

305
Q

Recognise the signs of perineal abscesses and fistulae on physical examination

A

Lump/nodule, tenderness, discharge

Small skin lesion near the anus (opening of the fistula)

A thickened area over the abscess/fistula may be felt

306
Q

Identify appropriate investigations for perineal abscesses and fistulae and interpret the results

A

DRE confirms the presence of the fissure

MRI: shows fistular tracts/deep abscesses

307
Q

Generate a management plan for perineal abscesses and fistulae

A

ABSCESS:
Prompt surgical drainage
Pain relief
Antibiotics usually not necessary

FISTULA:
Laying Open of Fistula
A probe is inserted to explore the fistula. Dye can be inserted into external opening to help find internal opening
Low Fistula - Fistulotomy. Care must be taken to prevent damage to the anal sphincter
High Fistula - Fistulotomy would cause INCONTINENCE so NOT performed. Seton - a non-absorbable suture that is threaded through the fistula and allows drainage

Antibiotics

308
Q

Identify the possible complications of perineal abscesses and fistulae and its management

A

Systemic infection, fissure, recurrence, scarring
Damage to internal anal sphincter
Incontinence
Persisting pain

309
Q

Summarise the prognosis for patients with perineal abscesses and fistulae

A

Abscess: Good if treated promptly – 31% can develop a fistula
Fistula: High recurrence rate without complete excision

310
Q

Define peritonitis

A

Inflammation of the peritoneum, can be primary or secondary, localised or generalised

311
Q

Explain the aetiology / risk factors of peritonitis

A

UGIT: malignancy, trauma, peptic ulcer, iatrogenic
LGIT: ischaemic bowel, diverticulitis, hernia, appendicitis
Hepatobiliary system: cholecystitis, malignancy, pancreatitis
Genitourinary tract: pelvic inflammation, malignancy

312
Q

Recognise the presenting symptoms of peritonitis

A

Abdominal pain, worsening

Anorexia, nausea and vomiting

313
Q

Recognise the signs of peritonitis on physical examination

A

Patient appears unwell and distressed; fever; tachycardia
Tenderness, guarding and rebound tenderness
Patient may lie with knees flexed to avoid abdominal movement

314
Q

Identify appropriate investigations for peritonitis and interpret the results

A

Bloods: FBC, U&Es, LFTs, MC&S
Imaging: AXR, erect CXR, USS, CT, MRI

315
Q

Generate a management plan for peritonitis

A

Medical: Third-generation cephalosporin,
Surgical: Exploratory surgery

316
Q

Identify the possible complications of peritonitis and its management

A

Sepsis, death

317
Q

Summarise the prognosis for patients with peritonitis

A

Main prognostic factor is renal dysfunction

318
Q

Define pilonidal sinus

A

A small hole, or tunnel, that develops at the top of the buttocks

An abnormal epithelium-lined tract filled with hair that opens onto the skin surface, most commonly in the natal cleft

319
Q

Explain the aetiology / risk factors of pilonidal sinus

A

Abnormal hair growth, that grows into the skin rather than out of it (caused by shed or sheared hairs penetrating the skin) inciting and inflammatory reaction and sinus development

Risk Factors 
sedentary life-style, obesity, friction 
Hirsutism  
Spending a long time sitting down  
Occupational (e.g. hairdressers may develop interdigital pilonidal sinus)
320
Q

Summarise the epidemiology of pilonidal sinus

A

COMMON

Affects 0.7% of young adults

321
Q

Recognise the presenting symptoms of pilonidal sinus

A

Boil-like lump, pain, swelling, redness, pus discharge
Painful natal cleft
Often recurrent

322
Q

Recognise the signs of pilonidal sinus on physical examination

A

Midline openings or pits between the buttocks
Hairs may protrude from the swelling
If infection or abscess, the swelling will become tender
It may be fluctuant and discharge pus or blood-stained fluid on compression

Fever, erythema, swelling, lump

323
Q

Identify appropriate investigations for pilonidal sinus and interpret the results

A

No real investigation, diagnosis made on examination

324
Q

Generate a management plan for pilonidal sinus

A

Advice:
• Should be kept dry and clean, and area kept hair-free
Medical:
• Antibiotics: If there is pus or an abscess
Surgical:
• Incision and drainage, under general anaesthetic (acute)
• Excision: removing the skin around the sinus (chronic)

325
Q

Identify the possible complications of pilonidal sinus and its management

A

Pain
Infection
Abscess
Recurrence

326
Q

Summarise the prognosis for patients with pilonidal sinus

A

Good, simply needs to be treated

327
Q

Define portal hypertension

A

Abnormally high pressure in the hepatic portal vein; an hepatic venous gradient pressure of >12mmHg

328
Q

Explain the aetiology / risk factors of portal hypertension

A

Pre-Hepatic:
- Congenital atresia or stenosis
- Portal vein thrombosis; splenic vein thrombosis
- Extrinsic compression e.g. tumours
Hepatic:
- Cirrhosis; chronic hepatitis
- Schistosomiasis; granulomata
Post-hepatic:
- Budd-Chiari syndrome (hepatic vein obstruction)
- Constrictive pericarditis; right heart failure
Other:
- Increased hepatic blood flow (splenomegaly)
- Idiopathic
Left-sided portal hypertension
- Rare, confined to left side of portal system; presents as gastric varices bleeding

329
Q

Summarise the epidemiology of portal hypertension

A

Common in liver disease

330
Q

Recognise the presenting symptoms of portal hypertension

A

For Liver disease:
- History of jaundice, alcohol consumption, blood transfusion (hep B or C susceptibility), family
history For complications:
- Malaena, lethargy, abdominal distension, abdominal pain and fever

331
Q

Recognise the signs of portal hypertension on physical examination

A

Dilated veins in anterior abdominal wall and caput medusa
Venous hum, loudest in inspiration
Splenomegaly; ascites

Signs of Portal Hypertension 
- Caput medusae  
- Splenomegaly 
- Ascites  
Signs of Liver Failure 
- Jaundice  
- Spider naevi 
- Palmar erythema 
- Confusion  
- Asterixis  
- Fetor hepaticus (breathe of the dead)
- Enlarged or small liver  
- Gynaecomastia  
- Testicular atrophy
332
Q

Identify appropriate investigations for portal hypertension and interpret the results

A 
Bloods: LFTs, U&amp;Es, FBC, glucose, clotting
Portal Hypertension Measurement: HVPG
Scans: USS, Doppler, CT/MRI
Endoscopy: for oesophageal varices
Biopsy: if indicated
333
Q

Generate a management plan for portal hypertension

A

Difficult to treat, except by treating cause
Drug:
- Beta Blockers (carvedilol) reduces portal pressure
- Nitrates reduces portal pressure
- Vasoactive drugs (terlipressin and octreotide) to assist in acute bleeding
Endoscopy:
- To detect, monitor and treat varices
Transjugular intrahepatic portosystemic shunt (TIPS)
- Using a shunt to connect portal and hepatic veins, decompressing the portal system
- Ascites, oesophageal varices and gastric varices
Surgery:
- Surgical portosystemic shunts

334
Q

Identify the possible complications of portal hypertension and its management

A

Bleeding, ascites, pulmonary problems, liver failure, hepatic encephalopathy, cirrhotic cardiomyopathy

335
Q

Summarise the prognosis for patients with portal hypertension

A

Depends on underlying disease, Child-Pugh score determines prognosis

336
Q

Define primary biliary cirrhosis

A

Chronic inflammatory liver disease of the bile system, leading to cholestasis and cirrhosis

337
Q

Explain the aetiology / risk factors of primary biliary cirrhosis

A

Unknown, autoimmune aetiology is likely

338
Q

Recognise the presenting symptoms of primary biliary cirrhosis

A

Can be an incidental finding (from detecting high ALP)
Insidious onset fatigue, weight loss and pruritus
Discomfort in the RUQ (rarely)
Can present with a complication, or associated conditions

339
Q

Recognise the signs of primary biliary cirrhosis on physical examination

A

Early: no signs
Late: jaundice, skin pigmentation, excoriation marks, xanthomas, xanthomata, hepatomegaly, ascites
- Liver disease signs (palmar erythema, spider naevi, clubbing)

340
Q

Identify appropriate investigations for primary biliary cirrhosis and interpret the results

A

Bloods: LFT (increased AlkPhos, GGT and bilirubin)
Anti-mitochondrial antibodies are hallmark feature
USS: exclude extrahepatic biliary obstruction
Liver Biopsy: chronic inflammatory cells and granulomas around intrahepatic bile ducts

341
Q

Define primary sclerosing cholangitis

A

Chronic cholestatic liver disease characterised by progressive inflammatory fibrosis and obliteration of intrahepatic and extrahepatic bile ducts

342
Q

Explain the aetiology / risk factors of primary sclerosing cholangitis

A

Unknown, possible genetic predisposition with toxic/infective triggers

343
Q

Summarise the epidemiology of primary sclerosing cholangitis

A

more common in males (60%
affects all ages
associated with IBD

344
Q

Recognise the presenting symptoms of primary sclerosing cholangitis

A

Can be asymptomatic and diagnosed after an incidental finding of increased AlkPhos
Intermittent jaundice, pruritus, RUQ pain, weight loss and fatigue
Episodic fever, rigors, is less common
History of UC and symptoms of complications

345
Q

Recognise the signs of primary sclerosing cholangitis on physical examination

A

May have no signs

Evidence of: jaundice, hepatosplenomegaly, spider naevi, palmar erythema and ascites

346
Q

Identify appropriate investigations for primary sclerosing cholangitis and interpret the results

A

Bloods: LFTs (increased AlkPhos, GGT, bilirubin and transaminases, decreased albumin)
Serology: immunoglobulin levels (increased IgG (children) and IgM (Adults))
ERCP: structuring and interspersed dilation of bile ducts
MRCP: non-invasive imaging
Liver Biopsy: confirm diagnosis, and allows staging

347
Q

Summarise the epidemiology of primary biliary cirrhosis

A

more common in females

onset mostly at middle age

348
Q

Define rectal prolapse

A

The protrusion of either the rectal mucosa or the entire wall of the rectum
Partial: only mucosa involvement
Complete: all layers of the rectal wall

349
Q

Explain the aetiology / risk factors of rectal prolapse

A

Risk Factors: increased intra-abdominal pressure, previous surgery, pelvic floor dysfunction

350
Q

Summarise the epidemiology of rectal prolapse

351
Q

Recognise the presenting symptoms of rectal prolapse

A

Due to a lax sphincter, prolonger straining, and related to chronic neurological and psychological disorders.
Risk Factors: increased intra-abdominal pressure, previous surgery, pelvic floor dysfunction

352
Q

Recognise the signs of rectal prolapse on physical examination

A

Protruding mass at anus, possible tenderness

353
Q

Identify appropriate investigations for rectal prolapse and interpret the results

A

Barium enema/colonoscopy: evaluate entire colon prior to surgery
Other investigations to assess underlying conditions (e.g. stool microscopy)

354
Q

Define ulcerative colitis

A

Chronic relapsing and remitting inflammatory condition affecting the large bowel

355
Q

Explain the aetiology / risk factors of ulcerative colitis

A

Unknown, suggested genetic susceptibility, family history component
inappropriate immune response in a genetically susceptible individual

356
Q

Summarise the epidemiology of ulcerative colitis

A

1:1500, common in Ashkenazi Jews and Caucasians
15-30s onset
smoking increases risk
NSAIDs may exacerbate

357
Q

Recognise the presenting symptoms of ulcerative colitis

A

Bloody diarrhoea, or mucous, tenesmus and urgency Weight loss, fever, abdominal pain before passing stool

358
Q

Recognise the signs of ulcerative colitis on physical examination

A

Iron-deficiency anaemia, dehydration, clubbing, abdominal tenderness, tachycardia DRE: blood, mucous, tenderness

359
Q

Identify appropriate investigations for ulcerative colitis and interpret the results

A

Bloods: FBC, ESR, CRP, LFTs (p-anca positive)
Stool: culture (exclude infectious colitis)
AXR: exclude toxic megacolon
Flexible sigmoidoscopy: determines severity, histological confirmation
Barium enema: mucosal ulceration with granular appearance

360
Q

Generate a management plan for ulcerative colitis

A

Observe activity markers:
- Haemoglobin, albumin, ESR, CRP and diarrhoea frequency
Acute Exacerbations:
- IV rehydration, IV corticosteroids, antibiotics
- Bowel rest, parenteral feeding, DVT prophylaxis
- Mild disease: topical/oral 5-ASA derivatives e.g. mesalazine/sulphasalazine
- Moderate/Severe disease: oral steroids and oral 5-ASA (sulphasalazine) and
immunosuppression (azathioprine, cyclosporine)
Advice:
- Patient education and support
- Treatment of complications
Surgical:
- Indicated if failure of medical treatment
- Proctocolectomy with ileostomy or an ileo-anal pouch formation

361
Q

Identify the possible complications of ulcerative colitis and its management

A

GI: haemorrhage, toxic megacolon, perforation, colonic carcinoma
Extra-GI: uveitis, arthropathy, renal calculi

362
Q

Summarise the prognosis for patients with ulcerative colitis

A

Relapsing and remitting condition: normal life expectancy
Poor Prognosis: ABCDE; albumin <30, blood PR, CRP raised, dilated loops of bowel, eight or more bowel movements per day, fever

363
Q

Define viral hepatitis

A

Inflammation of the liver, due to a viral cause

364
Q

Explain the aetiology / risk factors of viral hepatitis

A

Causes are hepatitis viruses, HAV, HBV, HCV, HDV, HEV, EBV, CMV, (malaria, Q fever, syphilis, yellow fever)
Hep A spread by faecal-oral route or shellfish
Hep B spread by blood products, IV drug abused and physical or sexual contact
Hep C spread by blood: transfusion, IV drug abuse, sexual contact. RF: male, older, high viral use, alcohol use, HIV, HBV

365
Q

Summarise the epidemiology of viral hepatitis

A

Incidence is declining
Hep A endemic in africa and S.America.
Hep B endemic in Far East, Africa and mediterranean

366
Q

Recognise the presenting symptoms of viral hepatitis

A

Acute Infection:
• Nausea and vomiting; myalgia, fatigue, malaise
• RUQ pain; change in smell or taste
• Photophobia and headache
Chronic infection:
• May be asymptomatic
Can lead to chronic hepatitis, cirrhosis and HCC

367
Q

Recognise the signs of viral hepatitis on physical examination

A

RUQ tenderness, fever, hepatomegaly

Later: Jaundice, hepatosplenomegaly, arthralgia, urticaria

368
Q

Identify appropriate investigations for viral hepatitis and interpret the results

A

Bloods: FBC, U&Es, LFTs, clotting factors, serology
Imaging: USS/CT/MRI to assess cirrhosis

369
Q

Generate a management plan for viral hepatitis

A 
HAV: 
	• Mainly symptomatic; avoid alcohol 
HBV: 
	• Advice: avoid unprotected sex, education 
	• Treat acute infection: mainly symptomatic 
HCV: 
	• Largely symptomatic; avoid excess alcohol 
	• Drug therapy: peginterferon 
HDV: 
	• Pegylated interferon alpha 
	• Liver transplant 
HEV: 
	• Mainly supportive, as HAV
370
Q

Identify the possible complications of viral hepatitis and its management

A

Cirrhosis, liver failure, Guillian-Barre syndrome, hepatitis, HCC

371
Q

Summarise the prognosis for patients with viral hepatitis

A

Poor without treatment, especially fatal in the elderly

372
Q

What type of bacteria is H.pylori?

A

helical-shaped gram-negative

373
Q

Define volvulus

A

Rotation of a loop of small bowel around the axis of its mesentery that results in bowel obstruction and potential ischaemia.
The areas usually affected:
- Sigmoid colon - 65%
- Caecum - 30%
- VOLVULUS NEONATORUM - occurs in neonates and typically affects the midgut

Long, and twisted colon, usually in the sigmoid colon

374
Q

Explain the aetiology / risk factors of volvulus

A

Full bowel twists on its mesenteric pedicle to create a closed-loop obstruction

Risk Factors: elderly, chronic constipation, megacolon

Risk Factors 
Adults 
- Long sigmoid colon 
- Long mesentery  
- Mobile caecum  
- Chronic constipation  
- Adhesions 
- Chagas disease 
- Parasitic infections  
Neonatal 
- Malrotation
375
Q

Summarise the epidemiology of volvulus

A

Leading cause of obstruction in lesser developed countries

376
Q

Recognise the presenting symptoms of volvulus

A

Sudden onset severe colicky pain, associated with a distended abdomen, complete/absolute constipation
Vomiting

There may be a history of transient attacks in which spontaneous reduction of the volvulus has occurred
Neonatal volvulus presents around 3 months

377
Q

Recognise the signs of volvulus on physical examination

A

Distended abdomen, non-tender, palpable mass may be present

Signs of bowel obstruction with abdominal distension and tenderness 
Absent or tinkling bowel sounds  
Fever  
Tachycardia  
Signs of dehydration
378
Q

Identify appropriate investigations for volvulus and interpret the results

A

AXR: shows signs of volvulus (coffee bean or embryo)

May need barium enema - show obstruction

379
Q

Define Wilson’s disease

A

An autosomal recessive disorder characterised by a reduced biliary excretion of copper, and accumulation in the liver and brain, especially in the basal ganglia

380
Q

Explain the aetiology / risk factors of Wilson’s disease

A

Gene responsible is on chromosome 13

Mutation in a gene on chromosome 13 that codes for copper transporting ATPase (ATP7B) in hepatocytes
This interferes with the transport of copper into the intracellular compartments for incorporation into caeruloplasmin (copper containing complex)
Caeruloplasmin is normally secreted into plasma or excreted in bile
Excess copper damages the hepatocyte mitochondria, leading to cell death and release of free copper into the plasma
This free copper then gets deposited in tissues and impairs tissue function

381
Q

Summarise the epidemiology of Wilson’s disease

A

Liver disease may present in children

Neurological disease usually presents in young adults

382
Q

Recognise the presenting symptoms of Wilson’s disease

A

Liver: (may present with hepatitis, liver failure or cirrhosis;) jaundice, easy bruising, variceal bleeding, encephalopathy
Neurological: dyskinesia, rigidity, tremor, dystonia, dysarthria, dysphagia, drooling, dementia, ataxia
Psychiatric: conduct disorders, personality changes and psychosis

383
Q

Recognise the signs of Wilson’s disease on physical examination

A

Liver: hepatosplenomegaly, jaundice, ascites/oedema, gynaecomastia
Neurological: (same as symptoms) dyskinesia, rigidity, tremor, dystonia, dysarthria, dysphagia, drooling, dementia, ataxia
Eyes: green/brown Kayser-Fleischer rings in the corneal limbus, sunflower cataract

384
Q

Identify appropriate investigations for Wilson’s disease and interpret the results

A

Bloods: LFTs, copper
24-hour urinary copper levels: increased
Liver biopsy: increased copper content
Genetic analysis: no simple genetic test to diagnose

Year 3 Conditions (8 decks)

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