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Y3 > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What is achalasia and what causes it?

A

An oesophageal motility disorder, characterised by loss of peristalsis and failure of relaxation of the lower oesophageal sphincter due to degeneration of the ganglion cells in the myenteric plexus

Unknown cause

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2
Q

When does achalasia usually present?

A

25-60yo

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3
Q

How does achalasia present?

A 
Insidious onset and gradual progression
Dysphagia - fluids and solids
Difficulty burping
Regurgitation - esp night
Substernal cramps - atypical chest pain
Heartburn
WL
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4
Q

How is achalasia investigated?

A

CXR:
Fluid level in dilated oesophagus
No gastric air bubble
Double R heart border - dilated oesophagus

Barium swallow:
Tapering dilated oesophagus - beak-shaped

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5
Q

What is alcoholic hepatitis?

A

Inflammatory liver injury caused by chronic heavy intake of alcohol

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6
Q

What causes alcoholic hepatitis?

A

Heavy alcohol intake for 15-20 years

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7
Q

What percentage of heavy drinkers develop alcoholic hepatitis?

A

10-35%

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8
Q

How does alcoholic hepatitis present?

A 
Many asymptomatic and undetected
Malaise
D+V
Low appetite
Epigastric to R hypochondria pain
Low grade fever

If severe: jaundice, abdo swelling, swollen ankles, GI bleed

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9
Q

How is alcoholic hepatitis investigated?

A
  1. BLOODS:
    High - WCC, bilirubin, AlkPh, AST/ALT, GGT
    Low - platelets, MCV, Hb, albumin
    Prolonged PT
  2. Percutaneous or transjugular biopsy
    - Centrilobular ballooning
    - Giant mitochondria
    - Degeneration and necrosis of hepatocytes
    - Steatosis
  3. US
  4. Upper GI endoscopy - ?varices
  5. EEG - slow-wave activity for encephalopathy
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10
Q

How is alcoholic hepatitis managed acutely?

A
  1. Thiamine, vit C, multivitamins
  2. Monitor and corect K, Mg, glucose
  3. Ensure adequate UO
  4. Treat encephalopathy - oral lactulose + phosphate enemas
  5. Treat ascites - diuretics (spiro + furosemide)
  6. Treat HRS - glypressin + N-acetylcysteine
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11
Q

How is malnutrition in alcoholic hepatitis managed?

A

Nutrition support - oral or NG
Increase calorie intake
Folic acid, B group, thiamine - start parentally, then orally
If severe: steroids short-term

Long-term - sort out alcohol dependence

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12
Q

What are the complications of alcoholic hepatitis?

A
  • Acute liver decompensation
  • Hepatorenal syndrome (renal failure secondary to advanced liver disease
  • Cirrhosis
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13
Q

What is the prognosis for alcoholic hepatitis?

A

Mortality
1st month - 10%
First year - 40%
If alcohol use continues, most –> cirrhosis in 1-3 years

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14
Q

What is an anal fissure?

A

Tear in the mucosa of the anal canal, just inside the anal margin

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15
Q

How are anal fissures classified?

A

Acute: present <6w
Chronic: present for >6w

Or primary + secondary

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16
Q

What can cause secondary anal fissures?

A

Constipation –> hard stool
IBD –> ulceration w inflammatory process
STD
Rectal malignancy

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17
Q

What causes primary anal fissures?

A

Unclear

Increased anal tone and ischaemia hindering healing process

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18
Q

Who are anal fissures most common in?

A

Below 40

350x more likely in women

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19
Q

How do anal fissures present?

A

Pain on defecation - like passing shards of glass
Pain may persist for several hours after
Bright fresh blood on passing stools

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20
Q

What are the signs of anal fissure O/E?

A

Hard abdo - faecal loading
Linear split of mucosa
Most are posterior to midline
DO NOT ATTEMPT DRE
Acute: clear edges, linear
Chronic: deeper, external skin tag at distal end
Secondary: more likely to be multiple, lateral, irregular demarcation

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21
Q

How are anal fissures managed?

A
  1. Keep stools regular and soft - adequate fluid intake, laxatives, 18-30g fibre/day
  2. Pain relief - analgesia prn, warm baths, GTN ointment (relax SM and decrease anal tone), topical anaesthetic if severe
  3. Topical diltiazem (CCB) –> vasodilation and SM relaxation
  4. Botox
  5. Internal sphincterectomy
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22
Q

What is a side-effect of GTN?

A

Headache

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23
Q

What is a side-effect of botox or surgery for anal fissures?

A

Temporary incontinence/flatus/faeces

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24
Q

What are the complications of anal fissures?

A
  • Tear fails to heal –> chronic, extensive scarring
  • Anal fistula
  • Anal stenosis - scar tissue
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25
Q

What is the prognosis for anal fissures?

A

Most heal in 2w with conservative management
Recurrence is common, 50% of those who use GTN
For secondary, depends on pathology

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26
Q

What is appendicitis?

A

Sudden inflammation of the appendix usually initiated by obstruction of the lumen

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27
Q

What causes appendicitis?

A

Gut organisms invade wall after luminal obstruction by lymphoid hyperplasia, faecolith or filarial worms

Leads to oedema, ischaemic necrosis, perforation

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28
Q

What is the most common cause of acute abdomen in the UK?

A

Appendicitis

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29
Q

When is appendicitis most common?

A

10-20yo

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30
Q

What are the symptoms of appendicitis?

A

Pain - early periumbilical pain –> RIF as peritoneum becomes involved, worse on moving, breathing, coughing

N+V + low appetite - usually constipated, low fever

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31
Q

What are the signs of appendicitis O/E?

A

Localised tenderness, guarding and rebound tenderness in RIF

Rovsing’s sign -> +ve if pain in RIF is greater than LIF when LIF pressed

Psoas sign -> pain on extending hip of retrocaecal appendix

Cope sign -> pain on flexion and internal rotation of right hip -> if appendix in close relation to obturator internus

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32
Q

What are the complications of appendicitis?

A

Rupture > faecal matter into peritoneal cavity > peritonitis

Appendix mass may form > surrounded by omentum > adheres

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33
Q

How is appendicitis managed?

A

Appendectomy

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34
Q

What is an appendectomy?

A

Surgical removal of the vermiform appendix

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35
Q

What are the indications for an appendectomy?

A

Acute appendicitis

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36
Q

What are the possible complications of an appendectomy?

A

Uncommon

Ileus
Haemorrhage
Wound infection
Local abscess
Pelvic abscess
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37
Q

What is autoimmune hepatitis?

A

An inflammatory liver disease of unknown cause characterised by suppressor T-cell defects with autoantibodies directed against hepatocyte surface antigens

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38
Q

How is autoimmune hepatitis classified?

A

Based on different autoantibodies

Type 1 (classic) - ANA, ASMA, AAA (anti-actin), ASLA (anti-soluble liver antigen)

Type 2 - ALKM-1 (liver/kidney microsomes), ALC-1

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39
Q

What causes autoimmune hepatitis?

A

Genetically predisposed
Environmental agent - virus or drugs
Leads to hepatocyte expression of HLA antigens
T-cell mediated AI attack of these hepatocytes
Chronic inflammatory changes
Lymphoid infiltration of portal tracts
Hepatocyte necrosis > fibrosis > cirrhosis

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40
Q

What are the risk factors for autoimmune hepatitis?

A

Personal Hx of Ai disesae

FHx

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41
Q

Who is autoimmune hepatitis most common in?

A

WOMEN
Bimodal: 10-30 and >40 yo
Mostly young or middle aged women

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42
Q

How does autoimmune hepatitis present?

A

Insidious onset

40% present with acute hepatitis + signs of AI disease:
Fever, malaise, low appetite, jaundice, n+v, RUQ pain, urticaria, pleurisy, pulmonary infiltration, glomerulonephritis

+- serum sickness - polyarthritis, arthralgia, maculopapular rash

+- keratoconjunctivitis sicca - dry eye syndrome

Everyone else - gradual jaundice or asymptomatic
Amenorrhoea common

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43
Q

What are the signs of autoimmune hepatitis O/E?

A

Stigmata of CLD
Spider naevi
Later - oedema, ascites, encephalopathy
Cushingoid features

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44
Q

What is Barrett’s oesophagus?

A

A change in the normal squamous epithelium of the oesophagus to specialised intestinal metaplasia (columnar)

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45
Q

What causes Barrett’s oesophagus?

A

Prolonged exposure or normal distal oesophageal squamous epithelium to GORD reflux (stomach acid)

Causes mucosal inflammation and erosion

Leads to replacement of mucosa with metaplastic columnar epithelium

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46
Q

What are the complications of Barrett’s oesophagus?

A

Oesophageal adenocarcinoma
Oesophageal stricture
QOL deficit

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47
Q

What are the risk factors for Barrett’s oesophagus?

A

3-5% of GORD sufferers get it

Increased risk if had it for longer/more frequent symptoms

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48
Q

Who usually gets Barrett’s oesophagus?

A

White men

Increasing age

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49
Q

How is Barrett’s oesophagus diagnosed?

A

Biopsy of endoscopically visible columnisation

Allows histological corroboration using Prague criteria

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50
Q

What are the symptoms of Barrett’s oesophagus?

A

Regurgitation

Heartburn

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51
Q

How is Barrett’s oesophagus managed?

A
  1. PPI + surveillance
  2. Anti-reflux surgery
    If dysplastic:
  3. Radiofrequency ablation +- mucosal resection
  4. Oesophagectomy
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52
Q

What is 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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53
Q

What happens when cirrhosis decompensates?

A 
Complications
Ascites
Jaundice
Encephalopathy
GI bleeding
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54
Q

What does cirrhosis look like histologically?

A

Loss of normal hepatic architecture
Bridging fibrosis
Nodular regeneration

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55
Q

What are the most common causes of cirrhosis?

A

UK: alcohol abuse
WW: HBV, HCV

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56
Q

What genetic diseases can cause cirrhosis?

A

Haemochromatosis
Alpha-1 antitrypsin deficiency
Wilson’s disease
CF

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57
Q

What are the causes of cirrhosis?

A

Alcohol abuse
HBV, HCV
Genetic: haemochromatosis, a1-AT def, Wilson’s CF
NASH
Chronic biliary disease - PBC, PSC
AI hepatitis
Hepatic vein events - Budd-Chiari, congestion
Drugs - methotrexate, amiodarone, methyldopa

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58
Q

What drugs can cause cirrhosis?

A

Methotrexate
Amiodarone
Methyldopa

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59
Q

What can trigger cirrhosis decompensation?

A 
Infection
GI bleeding
Constipation
High protein meal
Electrolyte imbalances
Alcohol/drugs
Tumour development
Portal vein thrombosis
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60
Q

How does cirrhosis present?

A

Early - non-specific - low appetite, weakness, WL, fatigue, n

Decreased liver synthetic function - easy bruising, abdo swelling, ankle oedema

Decreased detox function - jaundice, personality change, altered sleep, amenorrhoea

Portal HTN - abdo swelling, haematemesis, PR bleeding, melaena

May be asymp besides raised LFTs

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61
Q

What are the signs of CLD O/E?

A 
Nail clubbing
Palmar erythema
Spider nevi (angiomata)
Gynaecomastia
Feminising hair distribution
Testicular atrophy
Small irregular shrunken liver
Anaemia
Caput medusae
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62
Q

What are the signs of liver decompensation O/E?

A

Encephalopathy:
Drowsiness
Hyperventilation
Asterixis

Jaundice (excretory dysfunction)

Ascites (portal hypertension and hypoalbuminemia)
Leukonychia (hypoalbuminaemia)
Peripheral oedema (hypoalbuminaemia)

Bruising (coagulopathy)

Acid-base imbalance, most commonly respiratory alkalosis

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63
Q

How is cirrhosis investigated?

A
  1. BLOODS:
    FBC (low Hb, platelets due to hypersplenism)
    LFTs may be normal
    Raised transaminases/GGT/bili + low albumin
2. CLOTTING
Prolonged PT (due to reduced synthesis of clotting factors)
  1. IMAGING
    US/CT/MRI to detect complications
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64
Q

How is cirrhosis managed?

A

Treat cause
Avoid alcohol, sedatives, NSAIDs, drugs that affect liver
Monitor nutrition, if dietary intake is poor, give enterally

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65
Q

What is Coeliac disease?

A

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

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66
Q

What causes Coeliac disease?

A

HLA-DQ2/8

T-cell mediated

Prolamin (alcohol-soluble proteins in wheat, barley, rye, oats) intolerance causes villous atrophy and malasborption

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67
Q

What conditions is Coeliac disease associated with?

A 
AI disease
Dermatitis herpetiformis (chronic watery, itchy blisters on extensor surfaces)
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68
Q

Who is Coeliac disease most common in?

A

Irish

Children + 50-60yos

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69
Q

What are the symptoms of Coeliac disease?

A

1/3 asymptomatic

  • Steatorrhoea
  • Diarrhoea
  • Abdo pain, bloating
  • N+v, WL, fatigue, malaise
  • Failure to thrive in kids
  • Amenorrhoea
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70
Q

What are the signs of Coeliac disease O/E?

A
  • Aphthous ulcers, angular stomatitis
  • Dermatitis herpetiformis
  • Anaemia: pallor, weakness
  • Malnutrition: short, abdo distension, wasted buttock, decreased triceps skinfold thickness
  • Vit/min deficiencies: osteomalacia, easy bruising
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71
Q

How is Coeliac disease investigated?

A
  1. BLOODS - IDA (low Hb + MCV)/ macrocytic anaemia (if folate/B12 deficiency)
  2. IgA-tTg test/endomysial antibody (if Iga-tTg not available)
  3. Small bowel histology - presence of intra-epithelial lymphocytes, villous atrophy, and crypt hyperplasia
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72
Q

How is Coeliac disease managed?

A

Avoid gluten

Vitamin and mineral supplements

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73
Q

What are the complications of Coeliac disease?

A

Iron, folate, B12 deficiency
Osteomalacia
Ulcerative jujunoileitis
GI lymphoma

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74
Q

What is colonoscopy?

A

Endoscopic examination of large bowel and distal small bowel, using a fibre optic camera, passed on a flexible tube through the anus

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75
Q

What are the indications for colonoscopy?

A
  • GI haemorrhage
  • Unexplained changes in bowel habits/suspected malignancy
  • Diagnose CRC and IBD
  • Older patients: drop in hct (IDA)
  • Positive FOB
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76
Q

What are the possible complications of colonoscopy?

A

GI perforation 1:2000
Bleeding 2.6:1000
Death 3:100,000

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77
Q

What is Crohn’s disease?

A

Chronic granulomatous inflammatory disease that can affect any part of the GI tract

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78
Q

What are the characteristic features of Crohn’s disease?

A

Skip lesions

Transmural inflammation

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79
Q

What are the risk factors for Crohn’s disease?

A

Mutation of NOD2/CARD15 gene
Smoking x4
NSAIDs may exacerbate

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80
Q

When does Crohn’s disease incidence peak?

A

10-30y

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81
Q

Who usually gets Crohn’s disease?

A

10-30yo women

Lower prevalence in Asian

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82
Q

What are the signs of Crohn’s disease?

A

WL
Clubbing
Signs of anaemia - pallor, weakness
Abdo tenderness/masses
Aphthous ulcers in mouth
Perianal skin tags, fistulae, abscesses, anal strictures
Signs of complications - eye/joint/skin disease

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83
Q

What are the symptoms of Crohn’s disease?

A

Crampy abdo pain
Diarrhoea w urgency +- blood/steatorrhoea
Fever, malaise, Wl, low appetite

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84
Q

How is Crohn’s disease investigated?

A
  1. FBC - anaemia, leukocytosis/thrombocytosis, high ESR/CRP (inflammation), U+E, LFTs (low Alb)
  2. Iron studies - ?GI bleeding/malabsorption
  3. Low B12/folate
  4. Stool culture: exclude infectious colitis
  5. AXR: look for complications of toxic megacolon
  6. Erect CXR: if perforation risk
  7. Small bowel barium follow-through: fibrosis/strictures/deep ulceration
  8. Colonoscopy + biopsy: differentiate between CD and UC, monitor progression, malignancy
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85
Q

What is seen on colonoscopy of CD?

A

Mucosal oedema and ulceration - rose thorn fissures, cobblestone mucosa
Fistulae
Abscesses
Transmural chronic inflammation + infiltration of macrophages, lymphocytes, plasma cells

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86
Q

What are the complications of CD?

A

GI: SBO, toxic dilatation, haemorrhage, bowel stricture, perforation, fistulae, perianal fistulae and abscess, GI carcinoma, malabsorption

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87
Q

What are the extra-intestinal features of IBD?

A

Eyes: uveitis, episcleritis

Gallstones, kidney stones

Joints: arthropathy, sacroilitis, ankylosing spondylitis

Skin: erythema nodosum, pyoderma gangronosum

Amyloidosis

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88
Q

What is the prognosis for CD?

A

Chronic relapsing condition

2/3 need surgery eventually

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89
Q

How is CD managed?

A
  1. Steroids for acute exacerbations - IV hydrocortisone
  2. 5-ASA analogues (sulfasalazine, mesalazine) to induce remission
  3. Immunosuppression - azathioprine, methotrexate, 6-mercatopurine
  4. Anti-TNF agents - infliximab, adalimumab

Advice: stop smoking, dietician referral
Surgery if medical Tx doesn’t work

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90
Q

What is diverticular disease?

A

Diverticulae are present and symptomatic (associated with complications, eg haemorrhage, fistulae, infection)

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91
Q

What is a diverticulum?

A

Outpouching of colonic mucosa and submucosa through the muscular wall of the large bowel, usually at sites on entry of perforating arteries

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92
Q

What is diverticulosis?

A

Presence of asymptomatic diverticulae

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93
Q

What is diverticulitis?

A

Acute inflammation and infection of the diverticulae

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94
Q

What are the risk factors for diverticular disease?

A

Low fibre - loss of stool bulk > increased intraluminal pressures required to propel stool > mucosa must herniate through muscle layers

Over 50 years
Obesity

Little exercise
Red meat
Alcohol
Caffeine
Steroids
NSAIDs
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95
Q

Where are most diverticulae present?

A

Sigmoid colon

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96
Q

Who usually gets diverticular disease?

A

30% of Westerners have diverticulosis by age 60

Rare under 40

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97
Q

What is a symptom of diverticulosis?

A

Altered bowel habit

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98
Q

What are the signs of diverticulitis?

A

Localised tenderness
Palpable mass (sometimes)
Local/generalised peritonitis if perforation has occurred
+- reduced BS (may be increased w obstruction)

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99
Q

What are the symptoms of diverticular disease?

A

Bloating
Constipation
Mild LLQ pain

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100
Q

How does diverticulitis present?

A 
LLQ pain
Fever
Tachycardia
Localised/generalised peritonism
High WCC, CRP, ESR
Reduced BS
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101
Q

What are the complications of diverticulitis?

A
  1. Perforation > peritonitis
  2. Abscess - tender mass, persistent fever
  3. Fistulae - colovesicula (pneumaturia, faecaluria)/colovaginal (stool through vagina, freq vaginal infections, discharge)
  4. Stricture/obstruction - progressive fibrosis from recurrent episodes
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102
Q

How is diverticular disease investigated?

A
  1. BLOODS - FBC (high WCC, CRP in diverticulitis)
    Check clotting and XM if bleeding
  2. Barium enema +- air contrast - shows presence of diverticulae w saw-tooth appearance of lumen
  3. Flexi-sigmoidoscopy
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103
Q

How is diverticular disease managed?

A

Diverticulosis - high fibre diet, probiotics, anti-inflammatories (mesalazine)

GI bleeding - manage conservatively with IV rehydration, ABx and transfusions

Complications - surgery - resection + stoma

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104
Q

What is ERCP?

A

Technique that combines the use of endoscopy and fluoroscopy to diagnose and treat problems of the biliary/pancreatic ductal systems. Can inject a contrast medium into the biliary ducts and pancreas so they can be seen on radiographs

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105
Q

What are the indications for ERCP?

A 
Obstructive jaundice
Gallstones w dilated bile ducts on USS
Biliary strictures/suspected bile duct tumours
Suspected injury to bile ducts
Sphincter of Oddi dysfunction
Chronic pancreatitis
Suspected pancreatic tumour
Endoscopic sphincterotomy
Removal of stones
Insertion of bile duct stents
Dilation of strictures in PSC or anastomostic strictures on liver transplant
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106
Q

What are the possible complications of ERCP?

A

Pancreatitis
Intestinal perforation
Allergy to contrast dye (iodine)
Oversedation - low BP, resp depression, n+v

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107
Q

What is endoscopy - OGD?

A

Oesophagogastroduodenoscopy
Telescopic examination of the inside of the oesophagus, stomach and duodenum
Biopsies can also be taken

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108
Q

What are the indications for OGD?

A 
PUD diagnosis
Haematemesis
Melaena
Dyspepsia
Dysphagia
Coeliac disease - biopsy
Confirming suspected malignancy
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109
Q

What are the possible complications of OGD?

A

Minor - bleeding, infection

Major - perforation

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110
Q

What are gallstones

A

Stone formation in the gallbladder

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111
Q

What does bile contain?

A

Cholesterol
Phospholipids
Bile pigments - broken down Hb

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112
Q

What are the risk factors for gallstones?

A

5 Fs

Fair, fat, female, fertile, forty

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113
Q

Who usually gets gallstones?

A

Women 3x more in younger population

M=F after 65y

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114
Q

What are the signs of gallstones?

A

90% asymp

RF for being symptomatic - smoking, obesity

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115
Q

How are gallstones investigated?

A

USS

  • Acoustic shadow within gallbladder
  • Increased diameter of GB wall
  • Dilatation of biliary tree
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116
Q

What are the different types of gallstones?

A

PIGMENT STONES - 10&
Small, friable, irregular, radiolucent
Associated w haemolytic disorders - SCD, thalassaemia, spherocytosis

BLACK/BROWN CALCIUM BILIRUBINATE STONES
Increased bili due to haemolysis/cirrhosis
Or brown due to stasis and infection (bile duct infestation)

MIXED STONES
Ca, salts, pigments, cholesterol
Associated w increased age, F, obese, TPN, OCP, octreotide, FH, ethnicity, CD, ileal resection

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117
Q

What causes biliary colic?

A

Symptomatic gallstones with cystic duct obstruction or if passed into CBD

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118
Q

How does biliary colic present?

A 
Sudden onset, severe RUQ/epigastric pain, radiating to back
Constant
Worse after fatty meal
Associated n+v
May last several hours
Subsides spontaneously/with analgesia
\+- jaundice
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119
Q

What causes cholangitis?

A

Gallstone obstructs CBD
Leads to bile duct infection, biliary obstruction
Also caused by strictures, stenosis, parasites, tumours

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120
Q

What is cholangitis?

A

Infection of the biliary tree

Most commonly caused by obstruction

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121
Q

What is Charcot’s triad of cholangitis?

A

RUQ pain + jaundice + rigors

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122
Q

How does cholangitis present?

A 
Fever
RUQ pain
Jaundice
Mental status change
Tachycardia
Hypotension
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123
Q

How can you differentiate between biliary colic, acute cholecystitis and cholangitis?

A

Biliary colic: RUQ pain
Acute cholecystitis: RUQ pain + fever/high WCC
Cholangitis: RUQ pain + fever/high WCC + jaundice

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124
Q

How is cholangitis investigated?

A
  1. BLOODS
    High WCC/Ur/Cr/bili/transaminases/AlkPh/CRP
    Low platelets/K/Mg
    Culture: Gram -ve usually (sepsis)
  2. IMAGING
    ERCP/abdominal USS - dilated bile duct
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125
Q

How is cholangitis managed?

A
  1. IV ABx - piperacillin/tazobactam
  2. Non-operative biliary decompression - ERCP +- sphincterotomy and placement of drainage stent
  3. Opioid analgesics
  4. Lithotripsy if stones hard to remove
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126
Q

How are gallstones treated?

A

Cholecystectomy
ERCP with biliary sphincterotomy and stone extraction
Lithotripsy

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127
Q

What are the complications of gallstones in the GB and cystic duct?

A

Biliary colic
Acute/chronic cholecystitis
Mucococele: obstructed GB fills with mucus
Empyema: obstructed GB fills with pus
Carcinoma
Mirizzi’s syndrome: stone in GB presses on bile duct causing jaundice

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128
Q

What are the complications of gallstones in the bile ducts?

A

Obstructive jaundice
Cholangitis
Pancreatitis

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129
Q

What are the complications of gallstones in gut?

A

Gallstone ileus

Gallstone erodes through GB not duodenum, obstruction of terminal ileum

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130
Q

What is cholecystitis?

A

Acute inflammation of the gallbladder

Major complication of gallstones in cystic duct

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131
Q

What causes cholecystitis?

A

Complete cystic duct obstruction usually due to an impacted gallstone in the gallbladder neck or cystic duct, which leads to inflammation within the gallbladder wall

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132
Q

What are the risk factors for cholecystitis?

A 
Gallstones
Female
Increasing age
Obesity
Rapid WL
Pregnancy
CD
High lipids
133
Q

What are the symptoms of cholecystitis?

A

Continuous epigastric/RUQ pain
May refer to R shoulder due to diaphragmatic irritation
Vomiting
Fever

134
Q

What are the signs of cholecystitis?

A 
Tachycardia
Pyrexia
RUQ/epigastric tenderness
Local peritonism +- GB mass
Positive Murphy's sign - 2 fingers over RUQ, ask pt to breathe in deeply, +ve if this causes pain and arrest of inspiration as inflamed GB hits fingers (must not cause same pain in LUQ)
135
Q

How is cholecystitis investigated?

A
  1. BLOODS
    FBC (high WCC)
    High CRP
    LFTs - high bilirubin, AlkPh, GGT (cholestatic picture)
  2. RUQ USS - thick-walled, shrunken GB, pericholecystic fluid, stones, CBD dilatation
136
Q

How is cholecystitis managed?

A

Mild-moderate: NPO, IV fluids, ABx (cefuroxime), analgesia, close monitoring of blood pressure, pulse, and urinary output

Severe: urgent cholecystectomy + ITU

137
Q

What are the complications of cholecystitis?

A

Perforation
Gangrenous cholecystitis
Gallstone ileus

138
Q

What is cholecystectomy?

A

Surgical removal of the gallbladder

139
Q

What are the indications for cholecystectomy?

A
  1. Symptomatic cholelithiasis

2. Cholecystitis

140
Q

What are the possible complications of cholecystectomy?

A

Early - infection, haemorrhage, bile leak, injury to CBD/other bile ducts

Late - postcholecystectomy syndrome (persistent dyspeptic symptoms), port-site hernias

141
Q

What is GORD?

A

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

142
Q

What causes GORD?

A

Lower oesophageal sphincter hypotension due to:

  • Abdominal obesity / overeating
  • Gastric acid hypersecretion
  • Hiatus hernia
  • Slow gastric emptying
  • Smoking, alcohol, pregnancy
  • Surgery for achalasia
  • Drugs - tricyclics, anticholinergics, nitrates
  • Systemic sclerosis
143
Q

What are the RFs for GORD?

A
  • Abdominal obesity
  • Gastric acid hypersecretion
  • Hiatus hernia
  • Slow gastric emptying (fatty meal)
  • Overeating
  • Smoking, alcohol, pregnancy
  • Surgery for achalasia
  • Drugs - tricyclics, anticholinergics, nitrates
  • Systemic sclerosis
  • Anything causing increased intra-abdominal pressure or inadequate cardiac sphincter
144
Q

What are the symptoms of GORD?

A 
Heartburn - worse after meals, lying, alcohol, bending over
Burping
Acid brash: acid/bile regurg
Water brash: increased salivation
Painful swallowing

Nocturnal asthma
Chronic cough
Laryngitis - hoarseness
Sinusitis

145
Q

What are the signs of GORD O/E?

A

Sometimes epigastric tenderness
Wheeze
Dysphonia

146
Q

How is GORD investigated?

A
  1. Upper GI endoscopy, biopsy and cytological brushings - confirm oesophagitis, exclude malignancy (all patients over 45)
  2. Barium swallow - detect hiatus hernia, peptic stricture, extrinsic compression of oesophagus
  3. CXR - hiatus hernia - gastric bubble behind cardiac shadow
  4. 24h oesophageal pH monitoring
147
Q

How is GORD managed?

A
  1. Lifestyle advice - WL, elevate head of bed, stop smoking, lower fat meals
  2. Medical - antacids + alginates/H2 antagonists - ranitidine/PPI - lansoprazole
  3. Endoscopy - annual for Barrett’s oesophagus
  4. Surgery - anti-reflux surgery
  5. Nissen fundoplication - fundus of stomach wrapped around lower oesophagus and help with seromuscular sutures, helps reduce hiatus hernias and reflux
148
Q

What are the complications of GORD?

A 
Oesophageal ulceration
Peptic strictures
Anaemia
Barrett's oesophagus
Oesophageal adenocarcinoma
Asthma
Chronic laryngitis
149
Q

What is gastroenteritis?

A

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

150
Q

What causes gastroenteritis?

A

Viruses, bacteria, protozoa or toxins in contaminated food or water

Improperly cooked meat: S. aureus, C. perfringens
Old rice: B. cereus, S. aureus
Eggs/poultry: Salmonella
Milk/cheese: Listeria, Campylobacter
Canned food: Botulism

Inflammatory mechs: cytokine release > epithelial invasion > damage and bacteraemia (Shigella, Enteroinvasive E. Coli, Salmonella)

Non-inflamm mechs: production of enterotoxins, causing enterocytes to secrete water and electrolytes (V. Cholera, eneterotoxigenic E. coli)

151
Q

What are the risk factors for gastroenteritis?

A 
Recent travel
Poor personal hygiene
Undercooked food
Swimming in contaminated water
Exposure to others with GE
Compromised immune system - AIDS
Achlorhydria - absence of HCl in gastric secretions
152
Q

How does gastroenteritis present?

A 
Sudden onset n+v
Diarrhoea (bloody or watery)
Abdo pain
Fever
Malaise
153
Q

How does time on onset of gastroenteritis change depending on causative organism?

A

Toxins - early, 1-24h
Bacterial/viral/protozoal - 12h later
Parasites - days

154
Q

What are the signs of gastroenteritis O/E?

A

Diffuse abdo tenderness
Abdo distension
Increased BS
Severe: fever, dehydration, hypotension, peripheral shutdown

155
Q

How is gastroenteritis investigated?

A
  1. BLOODS - FBC/culture/UE
  2. Stool MCS
  3. AXR/US to exclude other causes
156
Q

How is gastroenteritis managed?

A

Bed rest
Fluid and electrolyte replacement
IV rehydration with severe vomiting
Most self-limiting

157
Q

What are the complications of gastroenteritis?

A 
Dehydration
Electrolyte imbalance
Prerenal failure
Secondary lactose intolerance, esp in kids
Sepsis, shock
HUS (E. Coli 0157)
GBS (Campylobacter)
Botulism (resp muscle weakness or paralysis)
158
Q

What is GI perforation?

A

Perforation of the wall of the GIT with spillage of bowel contents

Medical emergency, life-threatening

159
Q

What can cause perforation?

A 
Appendicitis
Cancer
IBD
Diverticulitis
GB disease
Peptic ulcer
Trauma - blunt or sharp
160
Q

How does perforation present?

A

Severe abdo pain, worse on palpation and mvmt
Chills and fever
NV
Bowel - pain at site then spreads across abdo
Gastric - burning epigastric pain, flatulence and dyspepsia
Duodenal - sudden epigastric pain, R of midline

161
Q

What are the signs of perforation O/E?

A

Rigid, silent, distended abdomen w tenderness and rebound tenderness
No flatus/motion
Distended abdomen

162
Q

How is perforation investigated?

A

Erect CXR - gas under diaphragm (70% perforated peptic ulcer)
AXR - abnormal gas shadows in tissues/Rigler’s sign (gas on either side of bowel wall)

163
Q

What is peritonitis?

A

Inflammation of the peritoneum

Perforation of the intestine causes the contents to leak into abdo cavity

164
Q

How does peritonitis present?

A 
Fatigue
Oliguria
SOB
Tachycardia
Dizziness
165
Q

What are the signs of peritonitis O/E?

A

Positive cough test - coughing causes pain in abdo
Tenderness +- rebound pain
Board like abdo rigidity
Absent BS

166
Q

What are haemorrhoids?

A

Disrupted and dilated anal cushions

167
Q

What causes haemorrhoids?

A

Gravity + increased anal tone + straining

168
Q

What are the risk factors for haemorrhoids?

A 
Constipation
Prolonged straining
Derangement of internal anal sphincter
Pregnancy
Portal HTN
169
Q

How do haemorrhoids present?

A

Bright red rectal bleeding
+- mucous, pruritis ani
+- anaemia
No WL, tenesmus, change in bowel habits

170
Q

How are haemorrhoids investigated?

A

Protoscopy or sigmoidoscopy to view internal haemorrhoids

171
Q

How are haemorrhoids managed?

A
  1. Dietary and lifestyle modification - 25-30g fibre/day
  2. Rectal hydrocortisone
  3. Rubber band ligation/sclerotherapy/IR photocoagulation/ligation/haemorrhoidopexy
  4. Surgical haemorrhoidectomy
172
Q

What are the complications of haemorrhoids?

A 
Anaemia
Thrombosis
Incarceration
Faecal incontinence
Pelvic sepsis
Anal stenosis
173
Q

What are the indications for haemorrhoidectomy?

A
  • Thrombosed external haemorrhoids which are diagnosed <72h

- Internal haemorrhoids - failed medical management

174
Q

What are the complications of haemorrhoidectomy?

A
  • Anal fistula/fissure
  • Continued constipation
  • PR bleeding
  • Excessive fluid discharge from rectum
  • Pyrexia
  • Unable to urinate or defecate
175
Q

What is a hernia?

A

A protrusion of a viscus through an abdominal opening

176
Q

What is a femoral hernia?

A

Bowel enters femoral canal, appears below and lateral to the pubic tubercle, medial to femoral pulse

177
Q

What causes femoral hernias?

A

Increased intraabdominal pressure with pressure on the weakened area (enlarged prostate, pregnancy, frequent cough, chronic constipation, intense workouts)

178
Q

Who are femoral hernias most common in?

A

Women 4x

179
Q

Where is the neck of a femoral hernia?

A

Inferior and lateral to pubic tubercle

180
Q

Where is an indirect inguinal hernia?

A

Passes through internal inguinal ring and out through external
Runs lateral to inferior epigastric vessels

181
Q

Where is a direct inguinal hernia?

A

Emerges through Hesselbach’s triangle
Pushes directly forward through posterior wall of inguinal canal, into a defect in abdominal wall
Runs medial to inferior epigastric vessels

182
Q

Who are indirect and direct inguinal hernias more common in?

A

Indirect - children due to failure of closure of inguinal canal during development

Direct - elderly

183
Q

What are the risk factors for inguinal hernias?

A 
Increased intra-abdo pressure:
Chronic cough
Constipation
Urinary obstruction
Heavy lifting
Ascites
Abdo surgery
Infants: prematurity, male
184
Q

How can hernias be investigated?

A

Ultrasound

185
Q

How are inguinal hernias managed?

A

Asymp: watchful waiting

Incarcerated/strangulated: urgent surgical repair + prophylactic ABx (cefazolin)

186
Q

How can you differentiate between femoral and inguinal hernias on examination?

A

Ask patient to cough
Femoral: inferior and lateral to pubic tubercle
Inguinal: superior and medial

187
Q

How can you differentiate between a direct and an indirect inguinal hernia on examination?

A

Reduce hernia
Occlude deep inguinal ring with 2 fingers
Ask pt to cough
If hernia is restrained –> indirect

188
Q

What is a hiatus hernia?

A

Herniation of part of the gastric cardia through the oesophageal aperture of the diaphragm

189
Q

What causes hiatus hernias?

A
  1. Widening of diaphragmatic hiatus
  2. Pulling up of stomach due to oesophageal shortening
  3. Pushing up of stomach due to increased intra-abdominal pressures
190
Q

What are the risk factors for hiatus hernias?

A 
Increasing age
Obesity
Pregnancy
Ascites
Genetic predisposition
Shortening of oesophagus, e.g. chronic oesophagitis
191
Q

Who are hiatus hernias most common in?

A

Obese women

People with Barrett’s oesophagus

192
Q

What do hiatus hernias increase your risk of?

A

6x oesophageal adenocarcinoma

193
Q

How do hiatus hernias present?

A 
Many asymptomatic
Heartburn
Flatulence
GORD
Dysphagia (rarely)
194
Q

In what type of hiatus hernias is acid reflux more common?

A

Sliding (gastro-oesophageal junction slides up into chest) - LOS is less competent

195
Q

How are hiatus hernias managed?

A

PPIs for symptomatic GORD

Surgical repair + Nissen’s fundoplication

196
Q

How are hiatus hernias investigated?

A

CXR - retrocardiac air bubble/normal

Upper GI series - stomach is partially/completely intrathoracic

197
Q

What is intestinal ischaemia?

A

A group of disorders that cause decreased blood flow to the GI tract

198
Q

What are the 3 main types of intestinal ischaemia?

A

Acute mesenteric
Chronic mesenteric
Chronic colonic

199
Q

What causes acute intestinal ischaemia?

A

ARTERIAL: thrombotic - atherosclerosis, embolic - MI, AF, endocarditis
NON-OCCLUSIVE: low-flow state, e.g. decreased CO
VENOUS: embolus, thrombosis - hypercoag disorders, tumours, infection
OTHER: trauma, vasculitis, radiotherapy, strangulation (volvulus, hernia)

200
Q

What causes chronic intestinal ischaemia?

A

Low-flow state + atheroma

201
Q

How does acute intestinal ischaemia present?

A

Moderate-severe colicky/constant poorly localised pain (RIF)

+ no abdo signs
+ shock

Physical findings out of proportion with degree of pain
Later stages - peritonism +- mass

202
Q

What is chronic mesenteric ischaemia?

A

AKA intestinal angina
Chronic atherosclerotic disease of vessels supplying intestine
Usually all 3 major mesenteric arteries involved

203
Q

Who usually gets the 3 different types of intestinal ischaemia?

A

Acute mesenteric - over 50s + young w RFs
Chronic mesenteric - over 60s
Chronic colonic - over 60s + young w non-CV causes (OCP+cocaine)

204
Q

What causes chronic mesenteric ischaemia?

A

Atherosclerotic causes

205
Q

How does chronic mesenteric ischaemia present?

A 
Postprandial severe, colicky pain
Weight loss (eating hurts)
Upper abdo bruit
\+- PR bleed, NV, malabsorption
Usually Hx of CV disease
206
Q

What is chronic colonic ischaemia also known as?

A

Ischaemic colitis

207
Q

What is chronic colonic ischaemia?

A

Compromise of blood flow to colon
Transverse and descending segments at risk due to supply from marginal branches and arterial/lymphatic watershed near splenic flexure

208
Q

What causes chronic colonic ischaemia?

A 
Thrombosis
Emboli
Decreased CO
Arrhythmias
Shock
Trauma
Strangulated hernia/volvulus
Surgery
Vasculitis - SLE
Coag disorders
209
Q

What are the signs of chronic colonic ischaemia?

A

Acute onset abdo pain (LIF)
NV
Loose motion w dark blood

210
Q

What causes small bowel obstruction?

A

Hernias

Adhesions

211
Q

What causes large bowel obstruction?

A

Colon cancer
Constipation
Diverticular stricture
Volvulus

212
Q

What are the rare causes of intestinal obstruction?

A 
Crohn's stricture
Gallstone ileus
Intussusception
TB
Foreign body
213
Q

What are the symptoms and signs of intestinal obstruction?

A 
N+V
Low appetite
Faeculent vomiting
Colic
Constipation
Abdo distension
Tinkling bowel sounds
214
Q

How do the symptoms of small and large bowel obstruction differ?

A

Small: vomiting occurs earlier, less distension, more pain
Large: more constant, more distension

215
Q

How is intestinal obstruction investigated?

A

AXR

Small bowel: central gas shadows with valvulae conniventes (completely cross lumen) + no gas in large bowel

Large bowel: peripheral gas shadows proximal to blockage but not in rectum + haustra do not cross lumen’s width

216
Q

What is ileus?

A

Functional obstruction from reduced peristalsis and bowel motility - no pain and absent bowel sounds

217
Q

What are the complications of intestinal obstruction?

A

Perforation
Sepsis
Death

218
Q

What is irritable bowel syndrome?

A 
A functional bowel disorder defined as recurrent episodes (in the absence of detectable organic pathology) of abdo pain/discomfort for more than 6 months of the previous year, associated with 2 of the following:
Altered stool passage
Abdo bloating
Symptoms worse on eating
Passage of mucous
219
Q

What are the risk factors for IBS?

A

Visceral sensory abnormalities
Gut motility problems
Stress
Food intolerance

220
Q

Who is IBS most common in?

A

Women 2x

Under 40

221
Q

What are the symptoms of IBS?

A

> 6m hx of abdo pain relieved by defecation/associated w altered stool form/bowel frequency >3 daily/<3/weekly

AND more than 2 of: urgency, incomplete evacuation, abdo bloating, mucous PR< tenesmus, worsening of symptoms after food

Also: nausea, bladder symptoms, backache

222
Q

How is IBS investigated?

A
  1. FBC: NORMAL (if anaemia, or anything raised –> not IBS)
  2. STOOL SAMPLE: normal (if not –> GE)
  3. Anti-tTG/anti-EMA: normal (raised in Coeliac)
  4. AXR: normal (no obstruction)
  5. Flexisig/colonoscopy: normal mucosa (not IBD)
223
Q

How is IBS managed?

A
  1. Lifestyle modification - less caffeine/lactose, more fibre
  2. Anti-diarrhoeals - loperamide
  3. Laxatives - ispaghula/lactulose
  4. Anti-spasmodics - dicycloverine/peppermint oil
224
Q

What are the complications of laparoscopic abdominal surgery?

A

Immediate - extraperitoneal insufflation, injury to viscera/vessels

Early - shoulder tip pain, wound infection, peritonitis, bile duct injury

Late - incisional hernia

225
Q

What is a liver abscess?

A

Purulent collections in the liver parenchyma that result from bacterial, fungal, or parasitic infection

226
Q

What causes liver abscesses?

A

Pyogenic liver abscess: often polymicrobial
E. Coli
Klebsiella
Streptococcus constellatus/anginosus/intermedius
Enterococcus
Anaerobes: Bacteroides fragilis, Fusobacterium necrophorum

60% by biliary tract disease - gallstones, strictures, cysts:
Amoebic: Entamoeba histolytica
Hyadatid: tapeworm Echinoccous granulosis
TB

227
Q

Where are pyogenic, amoebic and hyadatid liver abscesses most common?

A

Pyogenic - industralised world
Amoebic - Central and South America, Africa, Asia
Hyadatid - sheep-raring countries

228
Q

How do liver abscesses present?

A 
Fever, malaise, nausea, low appetite, night sweats, WL
Jaundice
Diarrhoea
PUO
RUQ/epigastric pain --> shoulder
Tender hepatomegaly
R pleural effusion - dull + reduced BS
229
Q

How are liver abscesses investigated?

A
  1. BLOODS
    FBC: leukocytosis, elevated neutrophil count, anaemia
    LFTs: high alk phos, mildly high aminotransferases and bilirubin, hypoalbuminaemia
    Culture
    PT/APTT: normal (check before doing aspiration)
  2. Liver US
  3. Contrast abdo CT: hypodense liver lesions
  4. Gram stain and culture of aspirated fluid
230
Q

What is a liver cyst?

A

A closed sac containing air, fluid or semi-solid material (not pus –> abscess)
Cells making shell of sac are abnormal

231
Q

What causes liver failure?

A

Infection: viral hepatitis (B,C,CMV) / yellow fever
Drugs: paracetamol OD, halthane, isoniazid
Toxins: Amanita phalloides mushroom, carbon tetrachloride
Vascular: Budd-Chiari syndrome, veno-occlusive disease
Others: alcohol, PBC, haemochromatosis, AI hep, a1AT deficiency, Wilson’s, fatty liver of pregnancy, malignancy

232
Q

What percentage of acute liver failure is due to paracetamol OD in the UK?

A

50%

233
Q

What are the symptoms of liver failure?

A

May be asymptomatic
Fever
Nausea
+- Jaundice

234
Q

What are the signs of liver failure?

A 
Jaundice
Hepatic encephalopathy
Fetor hepaticus (pear drops)
Asterixis
Constructional apraxia
\+- Ascites or splenomegaly
Bruising or bleeding for puncture sites of GIT
235
Q

What is a mallory-weiss tear?

A

Lacerations in region of gastro-oesophageal junction, often caused by retching

236
Q

How is acute liver failure investigated?

A
  1. LFTS - high bilirubin, high liver enzymes
  2. INR - high
  3. Urea and creatinine - high
  4. FBC - leukocytosis, anaemia, thrombocytopenia
  5. Hepatitis markers
237
Q

What are the risk factors for NASH?

A 
Alcohol
Obesity
DM
Hyperlipidaemia
Drugs - amiodarone, tamoxifen
Total parenteral nutrition
238
Q

How does NASH present?

A

Asymptomatic
+- Hepatomegaly

Splenomegaly + ascites –> cirrhosis not NASH

239
Q

How is NASH investigated?

A

LFTs - AST/ALT ratio < 1 (>2 –> alcohol use)

Liver biopsy - fatty liver

240
Q

How is NASH managed?

A 
Address cause
Weight reduction
Diabetic control
Alcohol abstinence
Drug cessation
241
Q

What is acute pancreatitis?

A

Acute inflammatory process of the pancreas

242
Q

What causes acute pancreatitis?

A

Insult results in activation of pancreatic proenzymes within duct/acini resulting in tissue damage and inflammation

Most common causes: alcohol (80%), gallstones

Drugs: steroids, azathioprine, thiazides, valproate, furosemide

Trauma, infection, abdo surgery, high lipids, hyperPT, anatomical, idiopathic

243
Q

How does acute pancreatitis present?

A

Gradual or sudden severe epigastric pain, radiates to back, relieved sitting forward, worse on movement
N+V
Decreased appetite
Hypovolaemia - low BP, sweating, tachycardia, dry mucous membranes, tachypnoea
Rigid abdomen
Cullen’s + Grey-Turner’s - haemorrhagic

244
Q

What are the risk factors for acute pancreatitis?

A 
Men 40-55 - alcohol
Women 50-70 - gallstones
Alcohol
High lipids
Drugs: steroids, azathioprine, thiazides, valproate, furosemide
ERCP
Trauma
SLE
Sjogren's
245
Q

How is acute pancreatitis investigated?

A 
BLOODS -
Serum lipase/amylase - 3x normal
AST/ALT - 3x normal - gallstone disease
FBC - leukocytosis + high hct (dehydration)/low hct (haemorrhage)
ABG - hypoxaemia

IMAGING-
AXR - isolated dilatation of a segment of gut adjacent to pancreas + cut-off sign
CXR - atelectasis + pleural effusion

246
Q

What is chronic pancreatitis?

A

Chronic inflammatory disease of the pancreas characterised by irreversible parenchymal atrophy and fibrosis leading to impaired endocrine and exocrine function and recurrent abdominal pain

247
Q

What are the causes of chronic pancreatitis?

A

Alcohol 70%
Idiopathic 20%
Rarely: familial, CF, haemochromatosis, pancreatic duct obstruction, hyperPTH congenital (pancreatic divisum), AI pancreatitis

248
Q

What are the symptoms of chronic pancreatitis?

A 
Recurrent severe epigastric pain radiating to back, better on sitting forward or heat, worse on eating/alcohol
Bloating
Steatorrhoea
WL
N+V
249
Q

What are the signs of chronic pancreatitis?

A

Epigastric tenderness

Signs of WL, malnutrition, DM

250
Q

How is chronic pancreatitis investigated?

A
  1. Blood glucose - raised
  2. CT - pancreatic calcifications, enlargement, ductal dilation, vascular complications
  3. Abdo US - structural changes
  4. Abdo XR - pancreatic calcifications
251
Q

How is chronic pancreatitis managed?

A
  1. Analgesia
  2. Lifestyle and dietary modifications - cut down alcohol, smoking
  3. Pancreatin (enzymes) + omeprazole
  4. Octreotide
  5. Antioxidants
252
Q

What are the complications of chronic pancreatitis?

A 
Pancreatic exocrine insufficiency
DM
Pancreatic calcifications
Pancreatic duct obstruction
Low-trauma fracture
253
Q

What causes PUD and gastritis?

A

Imbalance between damaging action of acid and pepsin and mucosal protective mechanisms

254
Q

What are the risk factors for PUD and gastritis?

A

H. pylori
Drugs - NSAIDs, steroids, SSRI
Reflux of duodenal contents into stomach
Stress

255
Q

What kind of PUD is more common?

A

Duodenal x4

256
Q

Who are duodenal and gastric ulcers more common in?

A

Duodenal: 30yos
Gastric: 50+

257
Q

What are the symptoms of PUD and gastritis?

A 
Epigastric pain relieved by antacids
Bloating
Fullness after meals
Heartburn
WL
Worse soon after eating - gastric
Worse hours later - duodenal
258
Q

How are PUD and gastritis investigated?

A 
Bloods:
FBC - anaemia
Amylase - normal
U+Es
Clotting screen - if GI bleeding
LFTs
Cross-match if actively bleeding

Endoscopy + brushings
Rockall scoring: assess severity after GI bleed
H. pylori testing: C-urea breath test, IgG against pylori, stool antigen test

259
Q

How are PUD and gastritis managed?

A
  1. Fluid resus
  2. IV omeprazole for UGI bleed
  3. Endoscopy - haemostasis by injection, sclerotherapy or electrocoagulation
  4. Surgery
  5. H.pylori eradication - triple therapy - PPI + clarithromycin + amoxicillin
  6. OR if not H. pylori - omeprazole/ranitidine (H2 ant), stop NSAID use
  7. Lifestyle - prevent stress, avoid trigger foods
260
Q

What are the complications of PUD and gastritis?

A 
Haemorrhage
Perforation
Obstruction
Pyloric stenosis due to scarring
Malignancy
261
Q

What is a perianal fistula?

A

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

262
Q

What causes perianal fistulae?

A

Bacteria tracking from anal glands, causing infection and then development of a fistula as a complication of an abscess

Or complication of cirrhosis

263
Q

What are the risk factors for perianal abscesses and fistulae?

A

IBD
DM
Malignancy
Cirrhosis

264
Q

What are the symptoms of perianal abscesses and fistulae?

A 
Constant throbbing pain in perineum
Intermittent discharge - mucous/faecal
Localised tender perineal mass/small skin lesion
Pain, swelling, redness
Fevers, general weakness
265
Q

How are perianal abscesses and fistulae managed?

A

Seton + antibiotics

Surgery - fistulotomy

266
Q

What is a pilonidal sinus?

A

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

267
Q

What caused pilonidal sinuses?

A

Shed/sheared hairs penetrating skin
Causes inflammatory reaction and sinus development
Intermittent negative pressure draws in more hair
Perpetuates cycle

268
Q

What are the risk factors for pilonidal sinuses?

A

Hirsutism + long time sitting

Hairdressers - interdigital sinuses

269
Q

How do pilonidal sinuses present?

A

Painful natal cleft
Discharge
Swelling

270
Q

How are pilonidal sinuses managed?

A

Surgical:
Incision + drainage
Packed w iodine-soaked dressings

Prevention:
Hygiene + hair removal

271
Q

What are the complications of pilonidal sinuses?

A

Pain
Infection
Abscess
Recurrence

272
Q

What is portal hypertension?

A

Abnormally high pressure in portal vein

273
Q

What causes portal hypertension?

A

Prehepatic: portal/splenic vein thrombosis

Hepatic: cirrhosis, schistosomiasis, sarcoid, myeloproliferative disease, congenital hepatic fibrosis

Post-hepatic: Budd-Chiari (hepatic vein thrombosis), congestive HF, constrictive pericarditis, veno-occlusive disease

274
Q

How does portal hypertension present?

A 
Signs of CLD
Haematemesis
PR bleeding/melaena
Oesophageal varices - upper GI bleed
Encephalopathy
Splenomegaly
Ascites/oedema
Caput medusa
275
Q

How is portal HTN investigated?

A

US - dilated portal vein

Hepatic venous pressure gradient = 5mmHg or more

276
Q

How is portal HTN managed?

A
  1. Portosystemic shunt
  2. TIPS
  3. Bleeding prevention - non-specific β-blockers, nitrate isosorbide mononitrate, terlipressin
  4. Ascites - salt restriction, spiro, paracentesis
  5. Encephalopathy - phosphate enemas, lactulose
277
Q

What is primary biliary cholangitis?

A

Chronic disease of the small intra-hepatic bile ducts

Intra-lobular bile ducts are damaged by chronic autoimmune granulomatous inflammation causing cholestasis which may lead to fibrosis, cirrhosis and portal HTN

278
Q

What causes PBC?

A

Unknown environmental triggers + genetic predisposition leading to loss of immune tolerance to self-mitochondrial proteins
Anti-mitochondrial antibodies

279
Q

What are the risk factors for PBC?

A 
Female x10
45-60yo
FHx
Many UTIs
Smoking
Other AI disease
280
Q

How does PBC present?

A 
Pruritis
Fatigue + daytime sleepiness
Dry eyes + mouth (associated Sjogren's)
Postural dizziness/blackouts
Hepatomegaly
281
Q

How is PBC investigated?

A
  1. BLOODS
    High AlkPh + GGT - cholestasis
    High bilirubin + low albumin - impaired liver synthetic function
    High ALT
  2. Abdo US - excludes obstructive lesion within visible bile ducts
  3. Antimitochondrial antibody/ANA immunofluorescence
282
Q

What is primary sclerosing cholangitis?

A

Chronic progressive cholestatic liver disease, characterised by inflammation and fibrosis of the intrahepatic and extrahepatic bile ducts, resulting in diffuse, multi-focal stricture formation

283
Q

Who does PSC commonly affect?

A

Young and middle-aged men with underlying IBD (mostly UC)

284
Q

How does PSC present?

A 
RUQ/epigastric pain
WL
Intermittent jaundice
Pruritis
Fatigue
Or asymptomatic
285
Q

How is PSC investigated?

A
  1. BLOODS: high AlkPh + GGT, slightly high transaminases, later on low Alb + high bili
  2. Serology: high IgG kids, IgM adults, ASM, ANA, pANCA
  3. ERCP: stricturing and dilation of intrahepatic bile ducts
  4. MRCP
  5. Liver biopsy: confirms Dx and allows staging
286
Q

What is rectal prolapse?

A

The mucosa (partial/type 1) or all layers (complete/type 2) protrude through the anus

287
Q

What causes rectal prolapse?

A

Lax sphincter or prolonged straining

288
Q

What are the risk factors for rectal prolapse?

A 
Increased intra-abdo pressures
Previous surgery
Pelvic floor dysfunction
Parasitic infections - schistosomiasis
Neuro disease
Psychiatric disease
289
Q

How does rectal prolapse present?

A 
Incontinence
Mass protruding through anus
Pain
Constipation
Mucus or rectal bleeding
290
Q

What is Wilson’s disease?

A

Inherited disorder of biliary copper excretion with too much copper in the liver and CNS

291
Q

What causes Wilson’s disease?

A

Genetic, autosomal recessive disorder of gene n Chr13 that codes for ATP7B (copper transporting ATPase)

Copper absorption and transport to liver is fine but incorporation into caeruloplasmin in hepatocytes and excretion into bile is impaired

Copper accumulates in liver - damages hepatocyte mitochondria - cell death - release of free copper into plasma - deposited in other tissues

292
Q

How does Wilson’s disease present?

A 
Hx of hepatitis
Tremor
Dysarthria: slurred
Dystonia in arms
Incoordination
Sloppy/small handwriting
Dysdiadochokinesis
Abnormal eye movements
Normal sensation, muscular strength and reflexes
Kayser-Fleischer rings
Hepatosplenomegaly, jaundice, ascites, gynaecomastia
293
Q

How is Wilson’s disease investigated?

A

LFTS: abnormal - raised aminotransferases + raised bilirubin (jaundice)/low bilirubin (liver failure)

294
Q

What is volvulus?

A

Rotation of a loop of bowel around the axis of its mesentery that results in bowel obstruction and potential ischaemia

295
Q

What causes volvulus?

A

Anatomical factors - long mesentery, adhesions, tumours

296
Q

What are the risk factors for volvulus?

A 
Long sigmoid colon and mesentery
Mobile caecum
Chronic constipation
Very high residue diet
Tumour
Adhesions
Chaga's disease of colon
Parasitic infections
297
Q

How does volvulus present?

A 
Severe colicky abdo pain and swelling
Absolute constipation
Later, vomiting
Distension
Absent/tinkling bowel sounds
Fever, tachycardia, dehydration
298
Q

How is volvulus investigated?

A

AXR - coffee bean sign
Erect CXR - air under diaphragm if perforated
Water-soluble contrast enema - shows site of obstruction
CT scan

299
Q

What is ulcerative colitis?

A

Relapsing and remitting inflammatory disorder of the colonic mucosa

300
Q

What causes UC?

A

Unknown but theory: autoimmune disease initiated by an inflammatory response to colonic bacteria

301
Q

Who usually presents with UC?

A

20-40 + 60 yos peak
Men more than women
Scandinavia + Northern Europe

302
Q

What are the risk factors for UC?

A

FHx of IBD

HLA-B27

303
Q

How does UC present?

A 
Rectal bleeding + mucous
Bloody diarrhoea
Abdo pain
Malnutrition
Urgency + tenesmus (rectal UC)

Extra-intestinal signs: clubbing, aphthous oral ulcers, erythema nodosum, pyoderma gangrenosum, conjunctivitis, episcleritis, iritis, arthritis, sacroilitis, ankylosing spondylitis, amyloidosis

304
Q

How is UC investigated?

A
  1. BLOODS:
    Low Hb/albumin
    High WCC/ESR/CRP
    LFTs, cultures, U+Es
  2. STOOL - exclude infectious colitis
  3. Faecal calprotectin - marks disease severity
  4. AXR: mucosal thickening, colonic dilatation
  5. Erect CXR: perforation
  6. Barium enema: lead-pipe pattern (no haustra)
  7. Colonoscopy/flexisig: inflammatory infiltrate, goblet cell depletion, glandular distortion, ulcers, crypt cell abscesses
305
Q

How is UC managed?

A

Mild - 5-ASA (sulfasalazine) + steroids (prednisolone)

Moderate - prednisolone + steroid enemas + sulfasalazine + immunosuppresion (azathioprine, cyclosporin, 6-mercatopurine, infliximab)

Sever - NBM + IV fluids + IV/PR hydrocortisone + blood transfusion + colectomy + parental nutrition

306
Q

What are the complications of UC?

A 
Perforation
Bleeding
Toxic dilatation of colon
Venous thrombosis
Colonic cancer
307
Q

What is hepatitis A?

A

RNA virus
Spread - faeco-oral/shellfish
Problem for travellers - endemic in Africa and S America
RFs - poor sanitation, unsafe water/food
Prodromal period: fever, malaise, no appetite, nausea, arthralgia, vomiting
Later: jaundice, adenopathy, dark urine, pale stool

308
Q

How is hepatitis A investigated?

A

Very high AST
High ALT
2-40 days post-exposure

High anti-HAV IgM from day 25
Anti-HAV IgG for life

Urine: high urobilinogen, bilirubin

309
Q

How is hepatitis A treated?

A

Supportive treatment

Immunisation

310
Q

What is the prognosis of hepatitis A?

A

Self-limiting
Recovery in 36 weeks
Chronicity doesn’t occur

311
Q

What is hepatitis E?

A

RNA virus
Similar to HAV
Older men, commoner than HAV in UK

312
Q

When does hepatitis E have a high mortality?

A

Pregnancy

313
Q

How is hepatitis E investigated?

A

Anti-HEV IgM and IgG

314
Q

What is hepatitis C?

A

ssRNA flavivirus spread via parental route: unscreened blood transfusion, IVDU, sexual, acupuncture tattoo, haemodilaysis, health workers

315
Q

What are the risk factors for progression of HCV?

A 
Male
Older
Increased viral load
Alcohol
HIV
HBV
316
Q

How does HCV present?

A

Mostly silent chronic infection

Sometimes jaundice + mild flu-like illness

317
Q

How is HCV investigated?

A

AST:ALT<1:1 until cirrhosis
Anti-HCV IgM and IgG
HCV-PCR - HCV RNA present
Liver biopsy

318
Q

How is HCV treated?

A

Stop alcohol
Supportive treatment
Protease inhibitors - boceprevir
PEG IFN-a and ribavirin

319
Q

What are the complications of HCV?

A

Fulminant liver failure

HCC

320
Q

What is hepatitis B?

A

dsDNA virus spread via blood products, IVDU, sexual, direct contact

321
Q

Where is HBV endemic?

A

Far East
Africa
Mediterranean

322
Q

How does HBV present?

A

Prodrome: malaise, headache, loss of appetite, N+V, diarrhoea, RUQ pain

+- Serum-sickness type illness: fever, arthralgia, polyarthritis, urticaria

Later jaundice w pale stool, dark urine

323
Q

How is HBV investigated?

A

Anti-HCV IgM (acute) and IgG (chronic)

HBsAg (surface antigen) 1-6 months after exposure

Liver biopsy

PCR

LFTs: high AST/ALT, bili, AlkPh

324
Q

How is HBV treated?

A

Stop alcohol
Immunise sexual contacts

Acute: symptomatic antiemetics, antipyretics, cholestyramine

Chronic: PEG IFNa-2a and lamivudine

325
Q

What are the side-effects of IFNa

A 
Flu-like chills
Myalgia
Headache
BM suppression
Depression
326
Q

What are the complications of HBV?

A

Leads to cirrhosis

Higher risk of HCC

327
Q

What is hepatitis D?

A

Incomplete RNA virus (needs HBV to assemble)

ssRNA virus coated with HBsAg

328
Q

How can HDV be prevented?

A

HBV vaccination

329
Q

How is HDV treated?

A

IFN-a - limited success

May need transplant

Y3 (20 decks)

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