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Diseases Flashcards

1
Q

Defective mucosal absorption is caused by what?

A
  • defective luminal digestion
  • mucosal disease
  • structural disorders
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2
Q

Name some common causes of malabsorption

A
  • coeliac disease
  • crohns disease
  • post infectious
  • biliary obstruction
  • cirrhosis
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3
Q

Name some uncommon causes of malabsorption

A
  • pancreatic cancer
  • parasites
  • bacterial overgrowth
  • drugs
  • short bowel (inc. resections
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4
Q

Name some malabsorptive states

A
  • protein
  • fat
  • carbohydrate
  • vitamin and minerals
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5
Q

Describe digestive protein malabsorption

A
  • partial or total gastrectomy (poor mixing)
  • exocrine pancreatic insufficiency
  • trypsinogen deficiency
  • congenital deficiency of intestinal enterokinase
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6
Q

Describe absorptive protein malabsorption

A
  • coeliac disease and tropical sprue
  • methionine malabsorption syndrome and blue diaper syndrome
  • short bowel syndrome
  • jejunoileal bypass
  • defects in neutral AA transporters
  • cystinuria
  • oculocerebral syndrome of lowe
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7
Q

Describe digestive fat malabsorption

A
  • less time to mix; gastric resection, autonomic neuropathy, amyloidosis
  • dec micelle formation, decrease bile acids synthesis / secretion; cirrhosis, biliary obstruction, CCK deficiency, small intestinal bacterial overgrowth
  • decreased lipolysis; chronic pancreatitis, cystic fibrosis, pancreatic ampullary tumours, low luminal pH, excessive calcium ingestion, lipase / co-lipase deficiency
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8
Q

Describe absorptive fat malabsorption

A
  • decreased chylomicron formation and / or mucosal absorption
  • coeliac disease, abetalipoproteinaemia, chylomicron retention disease
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9
Q

Describe post absorptive fat malabsorption

A
  • defective lymphatic transport

- primary intestinal lymphangicestasia, lymphoma, whipple disease, trauma, retroperitoneal fibrosis

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10
Q

Describe digestive carbohydrate malabsorption

A
  • severe pancreatic insufficiency

- alpha- amylase deficiency

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11
Q

Describe absorptive carbohydrate malabsorption

A
  • primary or acquired lactase deficiency

- post infectious lactase deficiency, coeliac disease, crohns, sucrase isomaltase deficiency, trehalase deficiency

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12
Q

What would cause vitamin B12 deficiency?

A
  • atrophic gastritis (impaired peptin / acid secretion)
  • deficiency of gastric intrinsic factor (pernicious anaemia / antrectomy)
  • pancreatic insufficiency (reduced release of B12 from R binding protein)
  • helminth infections
  • ileal crohn disease / resection
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13
Q

What could cause folic acid deficiency?

A
  • caused by diseases affecting the proximal small bowel
  • coeliac disease / whipple / tropical sprue
  • alcoholism
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14
Q

What could cause fat soluble vitamin (ADEK) deficiency?

A
  • anything that disrupts fat absorption will result in one / more deficiency
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15
Q

What could cause calcium deficiency?

A
  • selective deficiency can occur
  • renal disease / hypoparathyroidism
  • inborn defect in the vit D receptor
  • diseases that reduce intestinal surface area and / or cause formation of insoluble calcium soaps with long chain fatty acids
  • coeliac disease
  • bile acid deficiency
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16
Q

What would cause magnesium deficiency?

A
  • usually caused by loss of mucosal surface area and / or luminal binding by malabsorbed fatty acids
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17
Q

What could cause iron deficiency?

A
  • caused by reduced mucosal surface area but most often caused by GI bleeding
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18
Q

What could cause zinc deficiency?

A
  • acrodermatitis enteropathica

- defect in the zinc transport protein hZ1P4

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19
Q

What could cause copper deficiency?

A
  • menkes disease

- caused by an inherited disorder of cellular copper transport

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20
Q

What is coeliac disease?

A

Exposure to wheat, barley or rye induces a characteristic mucosal lesion

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21
Q

What causes coeliac disease?

A
  • intestinal antigen presenting cells in people expressing HLA-DQ2, or HLA-DQ8 bind with dietary gluten peptides in their antigen-binding grooves activate specific mucosal T lymphocytes cytokines mucosal damage
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22
Q

Describe the symptoms of coeliac disease

A
  • spectrum asymptomatic to nutritional deficiencies
  • weight loss
  • diarrhoea
  • excess flatus
  • abdominal discomfort
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23
Q

Describe the diagnosis of coeliac disease

A
  • IgA anti-tissue transglutaminase test (tTGA)

- biopsy confimative

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24
Q

Describe the treatment of coeliac disease

A

Gluten free diet

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25
Q

What causes lactose malabsorption?

A

Deficiency of lactase

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26
Q

Describe the symptoms of lactose malabsorption

A
  • history of the induction of diarrhoea
  • abdominal discomfort
  • flatulence
  • following ingestion of dairy products
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27
Q

Describe the diagnosis of lactose malabsorption

A
  • clinical
  • the diagnosis is confirmed by the lactose breath hydrogen test
  • an alternative is the oral lactose intolerance test
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28
Q

Describe the management of lactose malabsorption

A

Lactose free diet

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29
Q

What is tropical sprue caused by?

A

Colonisation of the intestine by an infectious agent or alterations in the intestinal bacterial flora induced by the exposure to another environmental agent

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30
Q

Describe the symptoms of tropical sprue

A
  • diarrhoea
  • steatorrhea
  • weight loss
  • nausea
  • anorexia
  • anaemia
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31
Q

Describe the treatment of tropical sprue

A
  • tetracycline

- folic acid

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32
Q

What causes whipples disease?

A
  • tropheryma whipplei

- multi system involvement in the frequency of HLA-B27

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33
Q

Describe the symptoms of whipples disease

A
  • weight loss
  • diarrhoea
  • steatorrhea
  • abdominal distention
  • arthritis
  • fever
  • nutritional deficiency symptoms
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34
Q

Describe the diagnosis of whipples disease

A
  • the diagnosis is established by demonstration of t. whipplei in involved tissues by microscopy
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35
Q

Describe the treatment of whipples disease

A

Antimicrobial

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36
Q

Describe crohns disease

A
  • crohn disease patients with extensive ileal involvement, extensive intestinal resections, enterocolic fistulas and stricture leading to small intestinal bacterial overgrowth may develop significant and occasionally devastating malabsorption
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37
Q

Describe the symptoms of crohns disease

A
  • abdominal pain
  • diarrhoea
  • fever and weight loss
  • abdominal tenderness
  • most classically in the right lower quadrant
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38
Q

Describe the diagnosis of crohns disease

A
  • endoscopy
  • barium imaging of the small bowel mucosal disease
  • including strictures
  • ulcerations
  • fistulae
  • CT
  • MRI
  • colonoscopy - punched out lesions
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39
Q

Describe the treatment of crohns disease

A
  • steroids
  • immunosuppressants
  • azathioprine 6-MP
  • biological therapy (anti TNF)
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40
Q

What are the risk factors for giardia lamblia (parasitic infection)

A
  • travel to areas where the water supply may be contaminated

- swimming in ponds

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41
Q

Name the symptoms of giardia lamblia parasitic infections

A
  • diarrhoea
  • flatulence
  • abdominal cramps
  • epigastric pain
  • nausea
  • 1/3 of symptomatic patients experience vomiting
  • significant malabsorption with steatorrhea and weight loss may develop
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42
Q

Describe lab investigations of giardia lamblia parasitic infection

A
  • stool examination for ova and parasites

- three separate stool samples increases the yield of positive examinations

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43
Q

Describe treatment of giardia lamblia parasitic infection

A

1 week of metronidazole

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44
Q

Describe small bowel bacterial overgrowth

A
  • diarrhoea, steatorrhea and macrocytic anaemia (B12)

- e coli or bacteroides

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45
Q

Name causes of small bowel bacterial overgrowth

A
  • diverticula, fistulas and strictures related to crohns disease
  • bypass surgeries functional stasis
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46
Q

Describe the lab tests for small bowel bacterial overgrowth

A
  • low cobalamin and high folate levels
  • aerobic and /or anaerobic colonic type bacteria in a jejunal aspirate obtained by intubation
  • bacterial overgrowth is best established by a schilling test
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47
Q

Describe the treatment of small bowel bacterial overgrowth

A
  • surgical correction of an anatomical blind loop

- tetracyclines 2-3 weeks

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48
Q

Describe acrodermatitis enteropathica

A
  • skin
  • autosomal recessive
  • impaired zinc uptake
  • rash, perioral, acral, alopecia
  • life long zinc supplements
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49
Q

Describe dermatitis herpetiformis

A
  • skin
  • may indicate coeliac disease
  • itchy blisters
  • extensor surfaces
  • sub epithelial IgA deposition
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50
Q

Glossitis and angular stomatitis indicates what

A
  • B vitamins

- iron

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51
Q

Spooning of nails indicates what?

A
  • iron (thyroid)
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52
Q

Name baseline investigation in GI

A
  • FBC
  • coagulation
  • LFTs
  • albumin
  • calcium / magnesium
  • stool culture
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53
Q

Describe oral ulceration

A
  • discontinuity in the oral mucosa
  • multiple local and systemic disorders can give rise to oral ulceration
  • presentation; solitary ulcer, multiple ulcers
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54
Q

Name an infective cause of solitary ulcers

A

TB - primary or secondary infection

Tertiary syphilis

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55
Q

Name the three types of multiple ulcers

A
  • major
  • minor
  • herpetiform
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56
Q

Describe bechets

A
  • multiple ulcers
  • multisystem condition
  • hereditary systemic vasculitis
  • almost identical oral ulcers as RAU
  • additionally, genital ulceration, uveitis, erythema nodosum and other systemic features
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57
Q

Describe oral signs of anaemia

A
  • mucosal pallor
  • oral ulceration
  • glossitis
  • angular chelitis
  • predisposition to candida
  • disturbed taste
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58
Q

Name some mucocutaneous disorders of multiple ulcers

A
  • lichen planus
  • vesicolobullous disease - pemphigus and pemphigoid
  • lupus erythematosus
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59
Q

Describe lichen planus

A
  • bilateral
  • asymptomatic
  • can affect the skin
  • potentially malignant
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60
Q

Describe the oral manifestations of lupus erythematosus

A
  • ulceration
  • white patches
  • red and white patches
  • similar in appearance to lichen planus
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61
Q

Describe VB disease - pemphigus vulgaris

A
  • oral lesions are the first manifestations (50-80% of cases)
  • oral lesions precede skin lesions by 1 year or more
  • painful extensive oral ulceration
  • preceded by blisters, rupture easily
  • mikolsky sign
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62
Q

Describe VB disease - pemphigoid

A
  • benign mucous membrane pemphigoid
  • blisters more likely to be observed
  • painful oral ulceration
  • affects mucous membrane of other organs eg eye
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63
Q

Pemphigoid has what type of bullae?

A

Sub epithelial

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64
Q

Pemphigus has what type of bullae?

A

Intraepithelial bullae

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65
Q

Name some GI diseases wit oral manifestations

A
  • crohns
  • ulcerative colitis
  • peutz jeghers
  • gardeners syndrome
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66
Q

Describe the oral manifestations of crohns disease

A
  • in 0.5-20% of cases
  • oral lesions may precede abdominal symptoms
  • features;
  • cobble stoning of mucosa
  • localised mucogingivitis
  • linear ulceration
  • tissue tags / polyps
  • diffuse swelling - commonly of the lips
  • pyostomatitis vegetans
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67
Q

Describe the oral manifestations of ulcerative colitis

A
  • oral ulceration
  • pyostomatitis vegetans
  • angular stomatitis g
  • reflects severity of intestinal disease; exacerbation and remission
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68
Q

Describe pigmentation

A
  • racial pigmentation
  • melanotic macules
  • malignancy
  • smoking
  • addisons disease; excess ACTH / MSH released from pituitary in response to reduced cortisol levels
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69
Q

What is xerostomia?

A

Dry mouth

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70
Q

Describe Sjogren syndrome

A
  • dry eyes and dry mouth
  • most commonly affects females
  • may primary or secondary
  • when secondary - associated with other autoimmune disease eg. rheumatoid arthritis
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71
Q

Describe oral maifestations of Sjogren syndrome

A
  • enlarged salivary glands
  • as a result of dry mouth;
  • increased caries
  • depapillated tongue, fissured
  • red dry wrinkled mucosa
  • increased predisposition to candida
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72
Q

Describe dental erosion

A
  • pH of stomach contents can go as low as 1
  • erosion on palatal surfaces of upper anterior teeth
  • GORD
  • also remember bulimia
  • may have been dietary cause or previous problem
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73
Q

Describe oral manifestations of leukaemia

A
  • gingival enlargement
  • petechiae
  • mucosal bleeding
  • ulceration
  • infiltration by malignant cells
  • boggy gingivae
  • presentation due to underlying immuno-compromise; candida, herpes infection, opportunistic infection
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74
Q

Describe oral manifestations of HIV

A
  • ulceration
  • Kaposi sarcoma
  • HPV lesions
  • salivary gland swelling
  • as a result of immunosuppression
  • increased risk of malignancy
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75
Q

What are the three main components of GORD?

A
  • incompetent LOS
  • poor oesophageal clearance
  • barrier function / visceral sensitivity
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76
Q

Name symptoms of GORD

A
  • heartburn
  • acid reflux
  • waterbrash
  • dysphagia
  • odynophagia
  • weight loss
  • chest pain
  • hoarseness
  • coughing
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77
Q

Describe the investigation of GORD

A
  • endoscopy
  • BA swallow
  • oesophageal manometry and pH studies
  • nuclear studies
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78
Q

What are the aims of management of GORD?

A
  • symptom relief
  • healing oesophagitis
  • prevent complications
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79
Q

Describe gastroparesis

A
  • delayed gastric emptying

- no physical obstruction

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80
Q

Describe symptoms of gastroparesis

A
  • feeling of fullness
  • nausea
  • vomiting
  • weight loss
  • upper abdominal pain
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81
Q

Describe causes of gastroparesis

A
  • idiopathic
  • diabetes mellitus
  • cannabis
  • medication eg. opiates, anticholinergics
  • systemic diseases eg. systemic sclerosis
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82
Q

Describe investigation of gastroparesis

A

Gastric emptying studies

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83
Q

Describe management of gastroparesis

A
  • removal of precipitating factors eg. drugs
  • liquid / sloppy diet
  • eat little and often
  • promotility agents
  • gastric pacemaker
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84
Q

What is dyspepsia?

A
  • symptom / constellation of symptoms
  • epigastric pain or burning (epigastric pain syndrome)
  • postprandial fullness (postprandial distress syndrome)
  • early satiety (postprandial distress syndrome)
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85
Q

Describe the organic causes of dyspepsia

A
  • peptic ulcer disease
  • drugs (esp NSAIDs, COX2 inhibitors)
  • gastric cancer
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86
Q

Name functional causes of dyspepsia

A
  • idiopathic, NU
  • no evidence of culprit structural disease (OGD, other tests)
  • associated with other functional gut disorders eg. IBS
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87
Q

Describe examination findings of dyspepsia

A
  • if uncomplicated; epigastric tenderness only

- if complicated; cachexia, mass, evidence of gastric outflow obstruction, peritonism

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88
Q

Describe the modern management of dyspepsia

A
  • in the absence of alarm symptoms
  • non-invasive test and treat strategy
  • check h pylori status
  • eradicate if infected
  • cures ulcer disease
  • removes risk of gastric cancer
  • if HP -ve treat with acid inhibition as required
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89
Q

Describe peptic ulcer disease

A
  • a common cause of organic dyspepsia
  • pain predominant dyspepsia (to back)
  • often also nocturnal
  • aggravated or relieved by eating
  • relapsing and remitting chronic illness
  • lower > higher socio-economic groups
  • family history common
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90
Q

Describe causes of peptic ulcer disease

A
  • h pylori
  • approx. 90% of DU
  • approx. 60% of GU
  • NSAIDs
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91
Q

Describe h pylori

A
  • acquired in infancy
  • gm-ve microaerophilic flagellated bacillus
  • oral oral / faecal oral spread
  • consequences of infection do not arise until later in life
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92
Q

Describe the consequences of h pylori

A
  1. no pathology - the majority
  2. peptic ulcer disease
  3. gastric cancer
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93
Q

Describe the diagnosis of h pylori

A
  • gastric biopsy; urease test, histology, culture / sensitivity
  • urease breath test
  • FAT faecal antigen test
  • serology (IgA antibodies), not accurate with increasing patient age
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94
Q

Describe treatment of peptic ulcer disease

A
  • all antisecretory therapy (PPI)
  • all tested for presence of h pylori
  • h pylori +ve, eradicate and confirm
  • h pylori -ve, antisecretory therapy
  • withdraw NSAIDs
  • lifestyle
  • non-Hp/non-NSAID ulcers, nutrition and optimise comorbidities
  • no firm dietary recommendations
  • surgery - infrequent
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95
Q

Describe eradication therapy of h pylori

A
  • triple therapy for 1 week commonest
  • PPI + amoxicillin 1g BD + clarithromycin 500mg BD
  • PPI + metronidazole 400mg BD + clarithromycin 350mg BD
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96
Q

Describe complications of peptic ulcer disease

A
  • anaemia
  • bleeding
  • perforation
  • gastric outlet / duodenal obstruction, fibrotic scar
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97
Q

Describe the post therapy follow up of duodenal ulcers

A
  • uncomplicated DU requires no f/u

- only if ongoing symptoms

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98
Q

Describe the post therapy follow up of gastric ulcers

A
  • f/u endoscopy at 6-8 weeks

- ensure healing and no malignancy

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99
Q

Name causes of upper GI bleeding

A
  • duodenal ulcer
  • gastric erosions
  • gastric ulcer
  • varices
  • Mallory Weiss tear
  • oesophagitis
  • erosive duodenitis
  • neoplasm
  • stomach ulcer
  • oesophageal ulcer
  • miscellaneous
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100
Q

How do you assess the severity of haemorrhage?

A
  • the 100 rule
  • systolic BP <100 mmhg
  • pulse >100 min
  • Hb <100g/l
  • age >60
  • comorbid disease
  • postural drop in blood pressure
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101
Q

Describe treatment of peptic ulcers

A
  • endoscopic treatment (high risk ulcers)
  • acid suppression (infusions)
  • surgery
  • h pylori eradication, secondary prevention
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102
Q

Describe endoscopic treatment of peptic ulcers

A
  • injection
  • heater probe coagulation
  • combinations
  • clips
  • haemospray
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103
Q

How does haemospray work?

A

When hemospray comes into contact with blood, the powder absorbs water, then acts both cohesively and adhesively, forming a mechanical barrier over the bleeding site

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104
Q

Describe causes of obstruction

A
  • within the lumen (gallstone, food, bezoar)
  • within the wall (tumour, crohns, radiation)
  • outside the wall (adhesions, herniation)
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105
Q

Describe the typical presentation of obstruction

A
  • distension
  • borborygmic
  • vomiting
  • pain
  • faeculent vomiting
  • presence of a cause
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106
Q

Describe investigations for obstruction

A
  • assessing the state of the patient
  • urinalysis
  • blood
  • gases
  • confirming diagnosis
  • AXR
  • contrast CT scan of abdomen
  • gastrograffin studies
  • identifying those who need surgery and those who will settle
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107
Q

Describe the surgical management of obstruction

A
  • laparotomy
  • operative principles; antibiotics, antithromboembolic measures, usually a midline incision, can be laparoscopic, find the obstruction by following collapsed or dilated bowel
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108
Q

Describe mesenteric ischaemia

A
  • embolus, thrombosis (arterial and venous)
  • chronic; SMA, cramps, like angina of the guts, atherosclerosis
  • acute; small bowel usually gets infarcted, colon lives (marginal artery)
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109
Q

Describe causes of mesenteric ischaemia

A
  • embolus usually from AF, forms in LA, stick in a narrow SMA
  • in situ thrombosis, virchows triad
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110
Q

Describe diagnosis of mesenteric ischaemia

A
  • pain out of proportion to the clinical findings
  • acidosis on gases (low pH, high H+ concentration, high BE)
  • lactate elevated
  • CRP may be normal
  • WCC may be elevated
  • CT angiogram
  • at laparotomy
  • intervene before your patient is moribund
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111
Q

Describe treatment of mesenteric ischaemia

A
  • quickly
  • prepare patient and family for the worst
  • resect if non-viable
  • re-anastomose or staple and planned return
  • if viable you can rarely perform an SMA embolectomy
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112
Q

Describe management of small bowel haemorrhage

A
  • ABC
  • exclude upper source
  • vascular malformations
  • ulceration
  • CT angiogram
  • can often be managed by interventional radiology
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113
Q

Describe meckels diverticulum

A
  • 60cm from IC valve
  • 2% of population
  • present before 2 years of age
  • usually incidental
  • remnant of the omphalomesenteric duct
  • complications; bleed, ulcerate, meckels diverticulitis, obstruction, malignant change
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114
Q

Describe the aetiology of appendicitis

A
  • no unifying hypothesis
  • obstructions of the lumen with faecolith
  • bacterial
  • viral
  • parasites
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115
Q

Describe the pathology of appendicitis

A
  • huge variation in macroscopic disease
  • lumen may or may not be occluded
  • mucosal inflammation
  • lymphoid hyperplasia
  • obstruction
  • build up of mucus and exudate
  • venous obstruction
  • ischaemia, bacterial invasion through wall
  • perforation
  • presence of inflammation in abdomen brings the greater omentum
  • small bowel adheres
  • phlegomonous mass
  • peritonitis can be fatal
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116
Q

Describe the signs and symptoms of appendicitis

A
  • central pain that migrates to RIF
  • anorexia
  • nausea
  • one or two vomits
  • may not have moved bowels
  • pelvic; vaguer pain localisation, rectal tenderness
  • elderly
  • mild pyrexia
  • mild tachycardia
  • localised pain in RIF
  • guarding
  • rebound
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117
Q

Describe the specific signs of appendicitis

A
  • Rosvings; pressing on the left causes pain on the right
  • psoas; patient keeps the right hip flexed as this lifts an inflamed appendix off the psoas
  • obturator; if appendix is touching obturator internus, flexing the hip and internally rotating will cause pain
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118
Q

Describe the differential diagnosis of appendicitis in children

A
  • gastroenteritis
  • mesenteric adenitis
  • meckels diverticulum
  • intussusception
  • Henoch schonlein purpura
  • lobar pneumonia
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119
Q

Describe the differential diagnosis of appendicitis in adults

A
  • terminal ileitis
  • ureteric colic
  • acute pyelonephritis
  • perforated ulcer
  • pancreatitis
  • rectus sheath haematoma
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120
Q

Describe the differential diagnosis of appendicitis in women

A
  • mittelschmerz
  • ovarian cyst
  • salpinigitis
  • ectopic pregnancy
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121
Q

Describe the differential diagnosis of appendicitis in the elderly

A
  • sigmoid diverticulitis
  • intestinal obstruction
  • carcinoma of the caecum
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122
Q

Describe investigations of appendicitis

A
  • clinical diagnosis
  • USS useful in women and kids
  • AXR to exclude other causes
  • bloods (CRP, WCC)
  • urinalysis
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123
Q

Describe the management of appendicitis

A
  • analgesia
  • antipyretics
  • theatre
  • antibiotics
  • appendicectomy
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124
Q

Describe the management of an appendix mass

A
  • antibiotics first line
  • can operate or not
  • theatre if fails or complicated; tachycardia, worsening pain, increase in size, vomiting or copious NG aspirates
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125
Q

Describe appendix abscess

A
  • not an appendix mass
  • usually delayed
  • usually has liquidised
  • radiological drains
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126
Q

Name neoplasms of the appendix

A
  • involved in normal adenocarcinoma of the caecum
  • pseudomyxoma peritonei
  • carcinoid
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127
Q

Describe carcinoid of the appendix

A
  • crypts of lieberkuhn
  • stains for chromagrannin
  • metastatic risk relates to size
  • if less than 1cm appendicectomy alone
  • if greater than 2cm completion right hemi
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128
Q

Define malnutrition

A

A state of nutrition in which a deficiency, excess or imbalance of energy, protein and other nutrients causes measurable adverse effects on tissue, body form (body shape, size and composition), function and clinical outcome

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129
Q

Name disease related causes of malnutrition

A
  • decreased intake
  • impaired digestion and or absorption
  • increased nutritional requirements
  • increased nutrient losses
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130
Q

Describe psychosocial causes of malnutrition

A
  • inappropriate food provision
  • lack of assistance
  • poor eating environment
  • self neglect
  • bereavement
  • inability to access food
  • deprivation
  • loneliness
  • lack of cooking skills or facilities
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131
Q

Describe the effects of starvation

A
  • decreases metabolic rate
  • weight; slow loss, almost all from fat stores
  • nitrogen losses decrease
  • hormones; early small increases in catecholamines, cortisol, GH, then slow fall. Insulin decreased
  • water and sodium; initial loss, late retention
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132
Q

Describe the effects of malnutrition

A
  • impaired immune responses
  • impaired wound healing
  • reduced muscle strength and fatigue
  • reduced respiratory muscle strength
  • inactivity, especially in bed bound patient
  • water and electrolyte disturbances
  • impaired thermoregulation
  • menstrual irregularities / amenorrhoea
  • impaired psycho-social function
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133
Q

What is anthropometry?

A
  • a form of nutritional assessment
  • mid arm muscle circumference
  • triceps
  • grip strength
  • refer to validated charts
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134
Q

Name some biochemical assessment of nutritional status

A
  • albumin
  • transferrin; synthesis reduced in protein restriction
  • transthyretin (prealbumin)
  • retinol binding protein
  • urinary creatinine; reflect s muscle mass
  • IGF1 ; reduced in acute and chronic malnutrition
  • micro nutrients
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135
Q

Describe parenteral nutrition

A
  • administration of nutrient solutions via a central or peripheral vein
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136
Q

Describe features of refeeding syndrome

A
  • hypokalaemia
  • hypophosphataemia
  • hypomagnesaemia
  • altered glucose metabolism
  • fluid overload
  • arrhythmias
  • altered level of consciousness
  • seizure
  • respiratory failure
  • cardiovascular collapse
  • death
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137
Q

What screening tool is used for malnutrition?

A

MUST

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138
Q

Describe intestinal failure

A
  • results from an inability to maintain adequate nutrition or fluid status via the intestines
  • can occur due to obstruction, dysmotility, surgical resection, congenital defect or disease associated loss of absorption
  • is characterised by the inability to maintain protein-energy, fluid, electrolyte or micronutrient balance
  • the reduction in function below the minimum necessary for the absorption of macronutrient and or water and electrolytes such that IV supplementation is required to maintain health a/o growth
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139
Q

Describe type 1 intestinal failure

A
  • short term
  • self limiting intestinal failure
  • wards; HDU/ICU
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140
Q

Describe type 2 intestinal failure

A
  • medium term
  • significant and prolonged PN support (>28days)
  • HDU/ICU wards
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141
Q

Describe type 3 intestinal failure

A
  • long term
  • chronic IF
  • long term PN support
  • wards to home
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142
Q

Name causes of type 1 intestinal failure

A
  • surgical ileus
  • critical illness
  • GI problems; vomiting, dysphagia, pancreatitis, GI obstruction, diarrhoea, oncology, chemo/ DXT, GVHD
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143
Q

Name causes of type 2 intestinal failure

A
  • post surgery awaiting reconstruction

- disaster, crohns, SMA, radiation, adhesions, fistulae

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144
Q

Name causes of type 3 intestinal failure

A
  • short bowel syndrome +/- other pathology
  • crohns +/- SBS
  • radiation +/- SBS
  • dysmotility
  • malabsorption, scleroderma, CV immunodeficiency
  • inoperable obstruction
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145
Q

Describe management of type 1 intestinal failure

A
  • common, short term
  • normal / moderately malnourished
  • replace fluid, correct electrolytes
  • parenteral nutrition if unable to tolerate oral food / fluids >7days post op
  • acid suppression; PPI
  • octreotide
  • alpha hydroxycholecalciferol to preserve Mg
  • intensive multi-disciplinary input
  • allow some diet / enteral feeding
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146
Q

Describe management of type 2 intestinal failure

A
  • septic patients
  • abdominal fistulae
  • perioperative who may develop a complication of feeding
  • weeks / months of care
  • parenteral +/- some enteral feeding
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147
Q

Describe short bowel syndrome

A
  • length of small bowel 250-1050cm
  • <200cm is short bowel
  • insufficient length of small bowel to meet nutritional needs without artificial nutritional support
  • most common indication for HPN
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148
Q

Describe types of short bowel

A
  • jejunostomy
  • jejuno-colic anastomosis
  • ileostomy
  • ileo-colic anastomosis
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149
Q

Describe complications of parenteral nutrition

A
  • sepsis
  • svc thrombosis
  • line fracture
  • line leakage
  • line migration
  • metabolic bone disease
  • nutrient toxicity / insufficiency
  • liver disturbance
  • metabolic disturbance
  • psycho-social
  • inappropriate usage
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150
Q

Describe treatment type 3 if

A
  • home parenteral nutrition
  • intestinal transplantation
  • glucagon like peptide 2 (teduglutide) treatment for SBS
  • bowel lengthening
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151
Q

Describe specialised types of endoscope

A
  • gastroscope
  • colonoscope
  • side viewing (ERCP) scope
  • enteroscope (push, double balloon)
  • capsule
  • endoscopic ultrasound
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152
Q

Endoscope can provide visual diagnosis for which conditions?

A
  • oesophagitis
  • gastritis
  • ulceration
  • coeliac disease
  • crohns disease
  • ulcerative disease
  • sclerosing cholangitis
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153
Q

Describe vascular abnormalities that can be viewed with endoscope

A
  • varices
  • ectatic blood vessels (GAVE, dieulafoy)
  • angiodysplasia
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154
Q

Describe variceal bleeding

A
  • life threatening medical emergency
  • ABC, resuscitate
  • injection fibrinogen
  • banding
  • histocryl glue
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155
Q

Define chrons disease

A
  • chronic inflammatory and ulcerating condition of the GI tract that can affect anywhere from the mouth to the anus
  • most common in the terminal ileum and colon
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156
Q

Who usually gets crohns disease?

A
  • young patients
  • can occur in children
  • more common in males
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157
Q

Name the sites of crohns disease

A
  • 2/3 patients have small bowel involvement only
  • 1/6 have colonic / anal disease
  • 1/6 have both
  • variable involvement of stomach, oesophagus and mouth
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158
Q

Describe the presentation of crohns disease

A
  • abdominal pain
  • small bowel obstruction
  • diarrhoea
  • bleeding PR
  • anaemia
  • weight loss
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159
Q

Describe the microscopic changes in crohns disease

A
  • chronic active colitis with granuloma formation
  • increased chronic inflammatory cells in the lamina propria and crypt branching with granulomas
  • large non-caseating granulomas
  • patchy chronic active colitis
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160
Q

Describe the pathology of crohns disease

A
  • segmental disease (patchy)
  • ileal and or colonic chronic active mucosal inflammation including; cryptitis, crypt abscesses
  • transmural inflammation
  • deep knife-life fissuring ulcers
  • granulomas, 50%, non-caseating
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161
Q

Describe the complications of crohns disease

A
  • malabsorption
  • fistulas
  • anal disease
  • intractable disease
  • bowel obstruction
  • perforation
  • malignancy
  • amyloidosis
  • rarely toxic megacolon
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162
Q

Describe malabsorption in relation to crohns

A
  • iatrogenic (short bowel syndrome) due to repeated resections and recurrences
  • hypoproteinemia, vitamin deficiency, anaemia of all types
  • gallstones (interrupted enterohepatic circulation)
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163
Q

Describe fistulas in relation to crohns disease

A
  • vesicocolic
  • enterocolic
  • gastrocolic
  • recto vaginal
  • tuboovarian abscess
  • blind loop syndrome
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164
Q

Describe anal disease in relation to crohns disease

A
  • sinuses
  • fissures
  • skin tags
  • abscesses
  • perineum falls apart
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165
Q

Describe intractable disease in relation to crohns disease

A
  • failure to tolerate or respond to medical therapy
  • continuous diarrhoea or pain
  • may require surgery, not curative
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166
Q

Describe the environmental triggers of crohns

A
  • smoking increases risk
  • infectious agents (viral, mycobacterial) cause similar pathology
  • vasculitis could explain the segmental distribution
  • sterile environment theory
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167
Q

Describe the abberant immune response of crohns

A
  • persistent activation of T cells and macrophages (failure to switch off)
  • excess proinflammatory cytokine production
  • may be alterable by changing intestinal microflora
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168
Q

Define ulcerative colitis

A
  • chronic inflammatory disorder confined to colon and rectum
  • mucosal and submucosal inflammation
  • unknown aetiology
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169
Q

Who typically gets ulcerative colitis?

A
  • young patients
  • peak incidence in the third decade
  • can present in the elderly
  • can occur in children
  • more common in males
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170
Q

Name the sites of ulcerative colitis

A
  • disease confined to the colon and rectum
  • nearly always involves the rectum
  • continuous and confluent extending proximally for varying lengths
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171
Q

Describe the clinical presentation of ulcerative colitis

A
  • diarrhoea
  • mucus
  • blood PR
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172
Q

Describe the pathology of ulcerative colitis

A
  • continuous, diffuse disease
  • rectal involvement, almost always
  • superficial ulceration and inflammation
  • chronic active colitis, cryptitis, crypt abscess
  • no granulomas
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173
Q

Describe the complications of ulcerative colitis

A
  • intractable disease
  • toxic megacolon
  • colorectal carcinoma
  • blood loss
  • electrolyte disturbance
  • anal fissures
  • eyes; uveitis
  • liver; primary sclerosing cholangitis
  • joints; arthritis, ank spondylitis
  • skin; pyoderma gangrenosum, erythema nodusum
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174
Q

Describe intractable disease in relation to ulcerative colitis

A
  • continuous diarrhoea
  • flares may be due to intercurrent infection by enteric bacteria or CMV
  • total colectomy
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175
Q

Describe toxic megacolon in relation to ulcerative colitis

A
  • acute or acute on chronic fulminant colitis
  • colon swells up to massive size
  • will rupture unless removed
  • emergency colectomy
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176
Q

Describe colorectal carcinoma in relation to ulcerative colitis

A
  • chronic inflammation leads to epithelial dysplasia and then carcinoma
  • risk increased if; pancolitis, disease longer than 10 yeas
  • requires surveillance
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177
Q

Describe the aberrant immune response of ulcerative colitis

A
  • persistent activation of T cells and macrophages
  • autoantibodies eg ANCA present
  • excess proinflammatory cytokine production and bystander damage due to neutrophilic inflammation
  • may be alterable by changing intestinal microflora
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178
Q

Describe the different types of colitis

A
  • ulcerative colitis
  • crohns colitis
  • collagenous colitis
  • lymphocytic colitis
  • radiation colitis
  • diversion colitis
  • drug induced
  • ischaemic colitis
  • antibiotic induced colitis
  • infective colitis
  • indeterminate colitis
  • necrotising enterocolitis
  • others
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179
Q

What is a polyp?

A
  • a polyp is a protrusion above an epithelial surface

- it is a tumour

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180
Q

Describe the differential diagnosis of a colonic polyp

A
  • adenoma
  • serrated polyp
  • polypoid carcinoma
  • other
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181
Q

Why must all adenomas be removed?

A

As they are all premalignant

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182
Q

Dukes staging predicts prognosis of what?

A

Colorectal carcinoma

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183
Q

Describe dukes staging

A
  • Dukes A; confined by muscularis propris
  • Dukes B; through muscularis propria
  • Dukes C; metastatic to lymph nodes
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184
Q

Describe the presenting complaint of left sided colorectal carcinoma

A
  • rectum, sigmoid, descending

- blood PR, altered bowel habit, obstruction

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185
Q

Describe the presenting complaint of right sided colorectal carcinoma

A
  • caecum, ascending

- anaemia, weight loss

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186
Q

Describe the pathology of the large bowel in terms of colorectal carcinoma

A
  • varied gross appearance (polypoid, structuring, ulcerating)
  • typical histopathological appearance (adenocarcinomas)
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187
Q

Describe the pattern of spread of colorectal carcinoma

A
  • local invasion; mesorectum, peritoneum, other organs
  • lymphatic spread; mesenteric nodes
  • hematogenous; liver, distant sites
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188
Q

Describe hereditary non polyposis coli

A
  • late onset
  • autosomal dominant
  • defect in DNA mismatch repair
  • inherited mutation in MLH-1, MSH-2, PMS-1 or MSH6 genes
  • right sided tumours
  • <100 polyps
  • mucinous tumours
  • crohns like inflammatory response
  • associated with gastric and endometrial carcinoma
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189
Q

Describe familial adenomatous polyposis

A
  • early onset
  • autosomal dominant
  • defect in tumour suppression
  • inherited mutation in FAP gene
  • throughout colon
  • > 100 polyps
  • adenocarcinoma NOS
  • no specific inflammatory response
  • associated with desmoid tumours and thyroid carcinoma
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190
Q

Name common large bowel diseases

A
  • carcinoma of the colon and rectum
  • colonic polyps
  • crohns colitis and ulcerative colitis
  • diverticular disease
  • functional disorders
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191
Q

Name less common large bowel disease

A
  • colonic volvulus
  • colonic angiodysplasia
  • ischaemic colitis
  • pseudo-obstruction
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192
Q

Describe diverticular disease

A
  • mucosal herniation through muscle coat
  • sigmoid colon
  • low fibre intake
  • incidental finding
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193
Q

Describe diagnosis of diverticulosis

A
  • clinical
  • barium enema
  • sigmoidoscopy
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194
Q

Describe the clinical features of diverticulitis

A
  • LIF pain / tenderness
  • septic
  • altered bowel habit
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195
Q

Describe complications of diverticular disease

A
  • pericolic abscess
  • perforation
  • haemorrhage
  • fistula
  • stricture
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196
Q

What classification is used for acute diverticulitis?

A
  • Hickney classification
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197
Q

Describe treatment of complex diverticulitis

A
  • hartmanns procedure
  • primary resection / anastomosis
  • percutaneous drainage
  • laparoscopic lavage and drainage
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198
Q

Describe causes of acute and chronic colitis

A
  • infective colitis
  • ulcerative colitis
  • crohns colitis
  • ischaemic colitis
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199
Q

Describe symptoms of acute and chronic colitis

A
  • diarrhoea +/- blood
  • abdominal cramps
  • dehydration
  • sepsis
  • weight loss, anaemia
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200
Q

Describe investigations of acute and chronic colitis

A
  • plain x-ray
  • sigmoidoscopy + biopsy
  • stool cultures
  • barium enema
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201
Q

Describe treatment of ulcerative colitis / crohns colitis

A
  • iv fluids
  • iv steroids; once infective / ischaemic colitis ruled out
  • GI rest
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202
Q

Describe ischaemic colitis

A
  • elderly
  • arteriopaths
  • acute or chronic occlusion
  • inferior mesenteric artery
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203
Q

Describe colonic angiodysplasia

A
  • submucosal lakes of blood
  • obscure cause of rectal bleeding
  • usually right side of colon
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204
Q

Describe diagnosis of colonic angiodysplasia

A
  • difficult
  • angiography
  • coloscopy
  • injection or surgical resection
205
Q

Describe treatment of colonic angiodysplasia

A
  • embolization
  • endoscopic ablation
  • surgical resection
206
Q

Name causes of large bowel obstruction

A
  • colorectal cancer
  • benign stricture
  • volvulus
207
Q

Name the cause of sigmoid volvulus

A
  • bowel twists on mesentery

- may become gangrenous

208
Q

Describe diagnosis of sigmoid volvulus

A
  • plain X-ray

- rectal contrast

209
Q

Describe treatment of sigmoid volvulus

A
  • flatus tube

- surgical resection

210
Q

Describe pseudo-obstruction

A
  • no real mechanical obstruction
  • elderly / debilitated
  • hypoxia
  • biochem
211
Q

Describe c diff

A
  • common cause of healthcare associated diarrhoea

- carried as part of normal bacteria flora in particularly in elderly (and infants)

212
Q

Describe the mechanism of action of c diff

A
  • organisms produces 2 toxins; toxin A (enterotoxin) and toxin B (cytotoxin)
213
Q

Describe the source / vehicle of infection of c diff

A
  • c diff often present in small numbers in bowel
  • infection occurs when antibiotics are prescribed that kill off normal competitive bowel flora and allows c diff to overgrow
  • organism produces spores that survive in the environment and are more resistant to disinfectants and the organism can be transmitted from one patient to another
214
Q

Describe symptoms of c diff

A
  • diarrhoea sometimes bloody
  • abdominal pain
  • severe cases may progress to pseudomembranous colitis or bowel perforation
215
Q

Describe management of c diff

A
  • depends on the severity assessment
  • less severe; oral metronidazole
  • severe = oral vancomycin
216
Q

Describe prevention of c diff

A
  • good antimicrobial prescribing stewardship is key
  • use narrow spectrum antibiotics where possible, avoid the 4 c’s
  • insolation of patients, handwashing and cleaning of the environment
217
Q

Describe the lab diagnosis of c diff

A
  • no on good test
  • screening test for presence of the organism (GDH)
  • if GDH positive, test for presence of toxin (A and B)
  • culture can be done if strain needs to by typed, not done routinely
218
Q

Describe the lab results for c diff

A
  • screening test neg; negative result
  • screening test +ve, toxin test +ve; positive result
  • screening test +ve, toxin test -ve ; indeterminate results, asses patient, repeat specimen
  • if repeat is indeterminate, clinical decision is required q
219
Q

Describe rotavirus

A
  • common cause of vomiting and diarrhoea in children <3 years
  • person person spread, direct or indirect
  • commoner in winter months
  • subclinical or mild in adults, can be severe in immunocompromised children
  • self limiting, lasts around 1 week
  • low infectious dose
  • survives in environment
  • billions shed in faeces when diarrhoea
  • increased absorption of fluids and increased secretion in bowel, causing dehydration
220
Q

Describe diagnosis and management of rotavirus

A
  • children may develop post-infection malabsorption, causing more diarrhoea
  • diagnosis by PCR test on faeces
  • management; rehydration is key
  • rotavirus vaccine (oral); live attenuated vaccine, excreted in faeces, 2 doses aged 2 & 3 months
221
Q

Describe norovirus

A
  • winter vomiting disease
  • affects all ages, highly infectious
  • faecal oral/ droplet routes of spread
  • person to person (or on contaminated food / water)
  • environmental survival on formite for days to weeks
  • low infectious dose required
  • community circulations is the reservoir
  • short incubation
  • sudden onset explosive d & v lasts 2-4 days
  • vomiting leads to widespread contamination of the environment
222
Q

Describe diagnosis and treatment of norovirus

A
  • diagnosis; faeces specimen or vomit swab for PCR test
  • treatment; rehydration is key, especially young, elderly
  • asymptomatic shedding occurs for to 48 hours post cessation of symptoms
  • outbreaks common
223
Q

Name other infections spread by faecal-oral route

A
  • hepatitis a and e
  • resistant bacteria that are carried in the GI tract, eg. vancomycin resistant enterococci, highly resistant gram negative organisms (CPEs)
224
Q

Describe aetiology of oral malignancy

A
  • tobacco
  • alcohol
  • diet and nutrition ‘
  • HPV
  • UVL
  • candida
  • syphilis / dental factors
225
Q

Name some potentially malignant lesions of the mouth

A
  • erythroplakia
  • erythroleukoplakia
  • leukoplakia
  • erosive lichen planus
  • submucous fibrosis
  • dyskeratosis congenita
  • sideropenic dysphagia
226
Q

Name warning signs for oral cancer

A
  • red / white lesions
  • ulcer
  • numb feeling, eg lip, face
  • unexplained pain in mouth or neck
  • change in voice
  • dysphagia
227
Q

Name other orofacial manifestations of cancer

A
  • drooping eye lid or facial palsy
  • fracture of mandible
  • double vision
  • blocked or bleeding from nose
  • facial swelling
228
Q

IBD consists of what?

A
  • 2 idiopathic chronic inflammatory diseases

- ulcerative colitis and crohns disease

229
Q

Describe the genetic factors of crohns

A
  • NOD2/ CARD15 (IBD-1)
  • disease susceptibility gene located on chromosome 16q12
  • a mutated form of NOD2 is found in 10-20% of Caucasian patients with crohns
  • homozygotes have 20-40 fold increased risk of disease
  • heterozygotes have 2-4 fold increased risk of disease
  • encodes a protein involved in bacterial recognition
230
Q

Describe the immunological factors of crohns

A
  • the immune system of normal intestine is geared towards tolerance to dietary antigens and commensal flora
  • innate immune responses are linked to the generation of corresponding adaptive immune responses
  • innate immunity; tight junctions regulate epithelial permeability, hydrophobic mucus protects the epithelial cell layer, defensins (cationic anti-microbial peptides) can be activated constitutively or in response to bacterial components, NOD2 contributes to normal mucosal defences
  • adaptive immunity; t lymphocytes are critical to the orchestration of adaptive mucosal immunity, normal conditions are characterised by a balance between effector and regulatory t cell responses. maladaptive responses may arise from either overactive effector t cells, absence of regulatory t cells
231
Q

Crohns disease is what type of immune response?

A
  • TH1 mediated disease
232
Q

Ulcerative colitis is what type of immune response?

A

Mixed TH1 / TH2 mediated disease /NKTC

233
Q

Describe antimicrobial activity in crohns

A
  • reduced antimicrobial activity in colonic crohns
234
Q

Describe smoking and IBD

A
  • smoking aggravates crohns disease

- protects against ulcerative colitis

235
Q

Describe ulcerative colitis

A
  • inflammation of colon of unknown aetiology
  • incidence 8-10/100000
  • peak incidence 20-30s
  • relapsing course
  • affects rectum extending proximally
236
Q

Describe ulcerative colitis symptoms

A
  • diarrhoea and bleeding
  • increased bowel frequency
  • urgency
  • tenesmus
  • incontinence
  • night rising
  • lower abdominal pain esp. lif
  • proctitis can cause constipation
237
Q

Describe the truelove and witt criteria

A
  • severe ulcerative colitis = 30% risk of colectomy
  • > 6 bloody stools / 24 hr
  • 1 or more of;
  • fever (>37.8)
  • tachycardia (>90/min)
  • anaemia (haemoglobin <10.5g/dl)
  • elevated ESR (>30mm/hr)
238
Q

Describe a plain AXR for ulcerative colitis

A
  • stool distribution; absent in inflamed colon
  • mucosal oedema / thumb printing
  • toxic megacolon; transverse >5.5cm caecum >9cm
239
Q

Describe endoscopy findings for ulcerative colitis

A
  • define extent
  • confluent inflammation extending proximally from anal margin to a transition zone
  • loss of vessel pattern
  • granular mucosa
  • contact bleeding
240
Q

Describe the histological findings of ulcerative colitis

A
  • crypt distortion and abscess
  • absence of goblet cells
  • affects mucosal layer only
241
Q

Describe the longterm complications of ulcerative colitis

A
  • increased risk of colorectal cancer
  • determined by; severity of inflammation, duration of disease, disease extent
  • extensive colitis (to beyond splenic flexure) at risk and require surveillance after 10 years of disease
242
Q

Describe extra-intestinal features of ulcerative colitis

A
  • mouth; stomatitis, aphthous ulcers
  • liver; steatosis
  • biliary tract; gallstones, sclerosing cholangitis
  • joints; spondylitis, sacrolitis, peripheral arthritis
  • circulation; phlebitis
  • skin; erythema nodosum, pyoderma gangrenosum
  • kidneys; stones, hydronephrosis, fistulae, urinary tract infection
  • eyes; uvetis, episcleritis
243
Q

Describe primary sclerosing cholangitis

A
  • chronic inflammatory disease of biliary tree
  • 80% have associated IBD
  • most asymptomatic OR itch, rigors
  • cholestatic LFTs
  • median time to death / liver transplant 10 years
244
Q

Describe the distribution of crohns

A
  • can affect any region of GI tract from mouth to anus
  • skip lesions
  • transmural inflammation
  • colonic crohns increasing in incidence
245
Q

Describe peri-anal disease

A
  • recurrent abscess formation
  • pain
  • can lead to fistula with persistent leakage
  • damaged sphincters
246
Q

Describe crohns symptoms

A
  • small intestine; abdominal cramp (peri-umbilical), diarrhoea, weight loss
  • colon; abdominal cramps (lower abdomen), diarrhoea with blood, weight loss
  • mouth; painful ulcers, swollen lips, angular cheilitis
  • anus; peri-anal abscess
247
Q

Describe the aims of IBD therapy

A
  • control inflammation and heal mucosa
  • restore normal bowel habit
  • improve quality of life
  • balance the effects of disease with side effects of treatment
  • avoid long term complications
  • be a good advocate for the patient
248
Q

Describe drug therapy for ulcerative colitis

A
  • 5ASA (mesalazine)
  • steroids
  • immunosuppressant
  • anti-TNF therapy
249
Q

Describe drug therapy for crohns disease

A
  • steroids
  • immunosuppressants
  • anti-TNF therapy
250
Q

Describe the mechanism of action of 5ASA

A
  • topical effect
  • anti-inflammatory properties
  • reduces risk of colon cancer
  • side effects; diarrhoea, idiosyncratic nephritis
251
Q

Name 5ASA drugs in use

A
  • sulphasalazine
  • balsalazide
  • mezavant
  • mesalazine
  • pH release (asacol)
  • delayed release (pentasa)
252
Q

Describe corticosteroid use in IBD

A
  • systemic anti-inflammatory properties
  • eg. prednisolone; oral / topical
  • budesonide
  • to induce remission
  • short course; high dose initially, reducing over 6-8 weeks
253
Q

Describe steroid side effects

A
  • avascular necrosis
  • osteoporosis
  • acne
  • thinning of skin
  • weight gain
  • diabetes
  • hypertension
  • cataracts
  • growth failure
254
Q

Describe azathioprine

A
  • slow onset of action (6 weeks)
  • TPMT activity contributes to toxicity - avoid co-prescription of allopurinol (XO inhibitor)
  • regular blood monitoring required
  • side effects; pancreatitis
  • leucopaenia
  • hepatitis
  • small risk of lymphoma, skin cancer
255
Q

Describe anti-TNF therapy

A
  • tumour necrosis factor alpha, proinflammatory cytokine
  • antibodies to TNF; chimeric (infliximab; IV infusion), humanised (adalimumab; S/C injection)
  • promote apoptosis of activated t lymphocytes
  • rapid onset of action
256
Q

Describe surgery for crohns

A
  • minimise amount of bowel resected
  • not curative
  • repeated resection of small intestine can result in short gut syndrome and requirement of lifelong total parenteral nutrition (reduced life expectancy)
257
Q

Describe surgery for ulcerative colitis

A
  • curative

- option of permanent ileostomy or restorative proctocolectomy and pouch

258
Q

Name elective operations for crohns

A
  • resection
  • stricturoplasty
  • fistulas
  • anal disease
259
Q

Describe elective operating for ulcerative colitis

A
  • proctocolectomy with end ileostomy

- proctocolectomy with ileorectal anastomosis

260
Q

Describe indications for elective surgery in UC

A
  • medically unresponsive disease
  • intolerability
  • dysplasia / malignancy
  • growth retardation in children
  • attempted resolution of extra-intestinal disease
261
Q

Describe a subtotal colectomy

A
  • first aid operation
  • subtotal colectomy
  • lap or open depending on expertise
  • rectal stump can be brought out as a mucous fistula
  • stapled and left in (riskier)
262
Q

Describe toxic megacolon

A
  • sepsis
  • distension
  • pain
  • requires decompression
  • may perforate
  • can be fatal
263
Q

Describe indications for surgery in crohns

A
  • stenosis causing obstruction
  • enterocutaneous fistulas
  • intra-abdominal fistulas
  • abscesses
  • bleeding (acute or chronic)
  • free perforation
264
Q

Describe fistulating disease and abscess

A
  • enterocutaneous
  • intra-abdominal
  • SNAP; sepsis, nutrition, anatomy, plan
265
Q

Describe intra-abdominal fistulae

A
  • may be occult
  • any organ can be affected (vagina, bladder)
  • resect en-bloc primary defect and close secondary organ
266
Q

Name psychological factors associated with GI disorders

A
  • current burdensome life events
  • abnormal relationships with parents
  • history or present abuse
  • anxiety
  • depression or low mood
  • neuroticism (anxious personality)
  • inadequate social support
  • difficulties in interpersonal relationships
267
Q

Describe globus

A
  • globus sensation, sensation of a lump in the throat
  • accounts for 4-6% of ENT clinic referrals
  • up to 46% of healthy people experience this symptoms
  • incidence peaks in middle age
268
Q

Name causes of globus sensation

A
  • foreign body
  • reflux
  • inflammation of pharynx
  • pharyngeal pouch
  • cancers
  • polled food syndrome / oral allergy syndrome
  • neurological conditions
269
Q

Describe globus management

A
  • reassurance
  • anti-reflux treatment
  • stopping smoking
  • referral to speech and language therapy
  • neck shoulder relaxation techniques and exercises
  • vocal hygiene
  • treatment for stress
  • antidepressant medication
  • CBT
270
Q

Describe functional dysphagia

A
  • the sensation of solid or liquid food sticking on the way down the oesophagus
  • prevalence not known
271
Q

Describe management of functional dysphagia

A
  • reassurance
  • dietary adjustments including avoidance of food that triggers dysphagia
  • advising carful chewing of food
  • avoiding fizzy drinks
272
Q

Describe management of IBS

A
  • diet modifications; consider fibre, caffeine, regular meals
  • exercise
  • reducing stress
  • medication; antispasmodics, laxatives, antimotility medicines, low dose antidepressants, reducing / stopping opiod analgesics
273
Q

Describe anorexia nervosa

A
  • significant weight loss (BMI <17.5 kg/m2)
  • in children; failure to make expected weight gain during growth
  • weight loss is self induced; avoidance of fatty foods, progressive dietary restriction, calorie counting / excessive weighing, self induce vomiting (russels sign), diuretics / laxatives / appetite suppressants
  • excessive exercise
274
Q

Describe the core psychopathology of anorexia nervosa

A
  • Intrusive, overvalued idea
  • obesity represents failure and chaos
  • slimness represents success and control
  • described as morbid fear of fatness, preoccupation with weight and shape
  • associated body image distortion, abdomen, thighs
275
Q

Describe the widespread endocrine abnormality associated with anorexia nervosa

A
  • decreased Na, K, PO4, insulin, glucose, thyroid (secondary to starvation)
  • cardiovascular / arrhythmias
  • bond health
  • amenorrhoea / loss of sexual interest / potency
  • elevated GY / cortisol/ cholesterol
276
Q

Describe bulimia nervosa

A
  • core psychopathology identical to anorexia nervosa
  • attempts to restrict intake fail > binges
  • low / normal/ increased weight
  • no endocrine abnormalities
  • 30% past history of anorexia
277
Q

Describe the treatment of anorexia nervosa and bulimia nervosa

A
  • establish therapeutic alliance
  • weight gain is essential
  • psychological interventions
  • antidepressants
  • antipsychotics
278
Q

Describe diagnosis of IBS

A
  • exclude organic disease relevant to patient
  • examination
  • nutritional status
  • anaemia
  • EIM of IBD
  • masses, PR
279
Q

Describe treatment of IBS

A
  • validate
  • reassure
  • inform
280
Q

Describe osmotic laxatives in IBS

A
  • polyethylene glycol
  • widely used
  • less s/e bloating, pain
  • NaH CO3, NaCl, KCl
  • prevents water absorption
  • improves constipation but not pain
  • one small adolescent study
  • lactulose
  • MgOH (milk of magnesia)
  • stimulant laxatives - avoid, only infrequent short term use
281
Q

Describe guanylate cyclase agonists

A
  • linaclotide (constella)
  • peptide agonist of guanylate cyclase 2C
  • increases intracellular cyclic GMP
  • increased intestinal secretion and transit
  • reduces abdominal pain
  • 2 large RCTS
  • longterm effects unknown
  • limited to failure / intolerance PEG laxatives
282
Q

Describe selective C-2 chloride channel activators

A
  • lubiprostone (amitiza, 24mcg od, 24mcg bd)
  • placebo for global IBS-C symptoms in women
  • IBS-C, CIC and opiate induce
  • bicyclic fatty acid derived from prostaglandin E
  • chloride rich secretion
  • soften stool, increase motility and promote SBMs
283
Q

Describe risk factors for STIs

A
  • <25 years old
  • changes sexual partner
  • non condom use
  • men who have sex with men
  • past history of STI
  • large urban areas
  • social deprivation
  • black ethnicity
284
Q

Describe rectal gonorrhoea

A
  • Neisseria gonorrhoea
  • transmission; direct contact of mucosal surface with infected secretions. For proctitis; anal sex, transmucosal spread, fomite
  • symptoms; short incubation period, lower abdo pain, diarrhoea, rectal bleeding, anal discharge, tenesmus, may have associated symptoms, may be asymptomatic
  • proctoscopy; inflamed mucosae, purulent exudate
  • complications; abscess formation, increased susceptibility / transmissibility of HIV
285
Q

Describe rectal chlamydia

A
  • symptoms; asymptomatic, milder than gonorrhoea, anal discomfort / itch, discharge, associated symptoms
  • proctoscopy; less sevee
  • gram stain rectal swab; CT, PCR
  • treatment; doxycycline, better clearance at rectal site, test of cure, comprehensive STI testing, public health interventions
286
Q

Describe primary and secondary syphilis

A
  • primary; solitary painless ulcer
  • secondary syphilis; mucosal patches and ulcers, mouth, anogenital, rectal, condylomata lata, systemic inflammation, hepatitis, procto-colitis
287
Q

Name risk factors for bowel cancer

A
  • older age
  • low intake of fibre
  • high intake of fat, sugar, alcohol, red meat, processed meats
  • obesity
  • smoking
  • lack of physical exercise
288
Q

Name signs and symptoms of right sided colorectal cancers

A
  • unexplained iron deficiency anaemia
  • persistent tiredness
  • a persistent and unexplained change in bowel habit
  • unexplained weight loss
  • abdominal pain (colicky in nature)
  • lump in the abdomen
289
Q

Describe signs and symptoms of left side and rectum colorectal cancers

A
  • rectal bleeding
  • feeling of incomplete emptying
  • worsening constipation
290
Q

Describe symptoms of intestinal obstruction

A
  • vomiting
  • pain
  • constipation
  • distension
  • complete obstruction
  • incomplete obstruction
291
Q

Describe vomiting in relation to intestinal obstruction

A
  • the more proximal the obstruction, the earlier vomiting develops
  • can occur even if nothing is taken by mouth, GI secretions continue to be produced, saliva, gastric, pancreatic, bile, small intestine
  • nature of vomitus gives clues to the level of obstruction
292
Q

How does the nature of the vomitus give clues to the level of obstruction

A
  • semi digested food eaten a day or two previously (no bile) suggest gastric outlet obstruction
  • copious bile stained fluid suggest upper small bowel obstruction
  • thicker, brown, foul-smelling vomitus (faeculent) suggests a more distal obstruction
293
Q

Describe constipation

A
  • propulsion of bowel contents is arrested
  • bowel gas is absorbed distal to the obstruction
  • absolute constipation (neither faeces or flatus passed rectally) is pathognomonic of bowel obstruction
294
Q

Describe physical signs of intestinal obstruction

A
  • dehydration (dry mouth, loss of skin turgor and elasticity)
  • abdominal distension
  • visible peristalsis
  • relative lack of abdominal tenderness
  • obstructing abdominal mass may be palpable
  • on percussion the centre of the abdomen tends to be resonant due to gaseous distension
  • groins must be examined for an obstructing hernia
  • bowel sounds are traditionally described as high-pitched and tinkling In practice they may be absent at the time of auscultation, echoing (cavernous quality) or may sound like water lapping against a boat
295
Q

Describe investigation of suspected bowel obstruction

A
  • most useful initial investigation is a supine abdominal x ray
  • bowel proximal to the obstruction is distended with gas
  • distended small bowel loops tend to lie in a central position and have valvulae coniventes
  • distended large bowel tends to lie in its anatomical position and has haustra coli
  • CT scan is often subsequently performed to confirm the diagnosis and look for a cause
  • transition point on CT scan with distended bowel proximal and collapsed bowel distal to the site of obstruction
296
Q

Name mechanical causes of bowel obstruction

A
  • adhesions or bands
  • incarcerated abdominal wall hernia
  • internal hernia
  • volvulus
  • tumour
  • inflammatory strictures
  • bolus obstruction
  • intussusception
297
Q

Describe adhesions or bands

A
  • congenital or resulting from previous abdominal surgery or peritonitis
298
Q

Describe volvulus

A
  • a mobile loop of bowel rotates causing obstruction at its neck
299
Q

Describe bolus obstruction

A
  • food bolus
  • impacted faeces
  • impacted gallstone ileus
  • trichobezoar
300
Q

Describe intussusception

A
  • a segment of bowel wall becomes telescoped into the segment distal to it
  • usually initiated by a mass in the bowel wall, enlargement of lymphatic tissue or tumour
301
Q

Describe bowel strangulation

A
  • a segment of bowel becomes trapped
  • venous return is obstructed
  • with rising local intra vascular pressure, subsequently arterial inflow is compromised
  • if strangulation is not relieved this will progress to infarction and perforation
  • pain over hernia
  • urgent surgical intervention
  • can occur in external hernia or volvulus
302
Q

Describe adynamic bowel obstruction

A
  • paralytic ileus

- pseudo-obstruction

303
Q

Describe paralytic ileus

A
  • disruption of the normal propulsive activity of the GI tract, due to failure of peristalsis
  • risk factors; recent GI surgery, inflammation with peritonitis, diabetic keto acidosis
  • symptoms and signs; similar to bowel obstruction and although pain and high pitched bowel sounds are less common
  • treatment; drip and suck while awaiting restoration of peristalsis
304
Q

Describe pseudo-obstruction (ogilvies syndrome)

A
  • acute dilatation of the colon in the absence of colonic obstruction in acutely unwell patients
  • associated with; hip replacement surgery, coronary artery bypass grafts, spinal, pneumonia, frail / elderly patients
305
Q

Describe the three major factors of cirrhosis

A
  • reduced liver blood flow
  • reduced metabolic function
  • reduced plasma proteins
306
Q

Describe moderate hepatic impairments

A
  • decrease renal clearance
  • effect on unbound drug masked by decrease protein binding
  • renal function reduced (creatinine and Cr clearance misleading)
307
Q

Describe consequences of moderate hepatic impairments

A
  • gut oedema, poor absorption
  • liver and kidney congestion, reduced function
  • gross oedema and ascites
  • CHF
308
Q

Describe nausea

A
  • subjective, highly unpleasant, sensation normally felt in throat and stomach as a sinking sensation
  • acute nausea interferes with mental and physical activity, often relieved by vomiting
  • chronic nauseas is greatly debilitating
  • nausea usually involves; pallor, sweating excessive salivation and relaxation of the stomach and lower oesophagus, upper intestinal contractions, forcing intestinal contents by reverse peristalsis into the stomach
  • nauseas usually precedes vomiting but either may occur in isolation
309
Q

Describe retching and vomiting

A
  • retching involves; rhythmic reverse peristalsis of the stomach and oesophagus, forceful, involuntary contraction of abdominal muscles and the diaphragm - cardiac portion of the stomach pushed into the thorax, upper intestinal contractions, forcing intestinal contents by reverse peristalsis into the stomach, pallor, sweating, excessive salivation
  • retching is dry, no efflux of vomitus
  • vomiting (emesis) is the forceful expulsion of gastric / intestinal contents out of the mouth
310
Q

Describe the overall events in vomiting

A
  • commences with forceful inspiration, reflex closure of the glottis and elevation of the soft palate to close off the airways and nasal passages
  • is not due to stomach contraction, stomach, oesophagus and associated sphincters are relaxed
  • vomiting is co-ordinated by the vomiting centre in the medulla oblongata of the brainstem
  • suspension of intestinal slow wave activity
  • retrograde contractions from ileum to stomach
  • suspension of breathing (closed glottis, prevents aspiration)
  • relaxation of LOS- contraction of diaphragm and abdominal muscles compresses stomach
  • ejection of gastric contents through open UOS
  • repeats of the cycle
  • vomiting is frequently preceded by profuse salivation, sweating, elevated heart rate and the sensation of nausea
311
Q

Describe the vomiting centre

A
  • a historically useful term, but not a discrete anatomical centre
  • instead a group of interconnected neurones within the medulla that are driven by a central pattern generator (CPG) that in turn receives input from the NTS
312
Q

Describe the consequences of severe vomiting

A
  • dehydration
  • loss of gastric protons and chloride (causes hypochloraemic metabolic alkalosis, raising blood pH)
  • hypokalaemia, mediated by the kidney, proton loss is accompanied by potassium excretion
  • rarely, loss of duodenal bicarbonate may cause metabolic acidosis
  • rarely, oesophageal damage (mallor-weiss tear)
313
Q

Describe drug and radiation induced emesis

A
  • many classes of drug (or treatments) predictably cause nausea and vomiting
  • cancer chemotherapy (eg. cisplatin, doxorubicin) and radiotherapy (release of 5-HT and substance P from enterochromaffin cells in the gut)
  • operations involving the administration of a general anaesthetic (post-operative nausea and vomiting)
  • agents with dopamine agonist properties (eg. levodopa used in parkinsons disease) dopamine D2 receptors are prevalent in the CTZ
  • morphine and other opiate analgesics (tolerance develops)
  • cardiac glycosides (eg. digoxin)
  • drugs enhancing 5-HT function (eg. SSRIs, 5-HT3 receptors are prevalent in the CTZ)
314
Q

Describe 5-HT3 receptor antagonists - setrons (eg. ondansetron, palonsetron)

A
  • used to suppress chemotherapy and radiation induced emesis and post-operative nausea and vomiting
  • block peripheral and central 5-HT3 receptors (cat ion selective ion channels)
  • reduce acute nausea, retching and vomiting in cancer patients receiving emetogenic treatments (day 1)
  • less effective during subsequent treatments (delayed phase), improved by the addition of a corticosteroid (mechanism uncertain) and a neurokinin 1 (NK1) receptor antagonist
  • not effective against motion sickness, or vomiting induced by agents increasing dopaminergic transmission
  • generally well tolerated, most common unwanted effects are constipation and headaches
315
Q

Describe muscarinic acetylcholine receptor antagonists (Eg. hyoscine / scopolamine)

A
  • used for prophylaxis and treatment of motion sickness (can be delivered by transdermal patch )
  • probably block muscarinic acetylcholine receptors at multiple sites (eg. vestibular nuclei, NTS, vomiting centre)
  • direct inhibition of GI movements and relaxation of the GI tract may contribute(modestly) to anti-emetic effects
  • have numerous unwanted effects resulting from blockade of the parasympathetic ANS (eg. blurred vision, urinary retention, dry mouth) and centrally mediated sedation
316
Q

Histamine H1 receptor antagonists (eg. cyclizine, cinnarizine and many others)

A
  • many agents in this class also exert significant blockade of muscarinic receptors that probably contributes to their activity
  • used for prophylaxis and treatment of motion sickness and acute labyrinthitis and nausea and vomiting caused by irritants in the stomach, less effective against substances that act directly on the CTZ
  • action attributed to the blockade of H1, receptors in vestibular nuclei and NTS
  • generally cause CNS depression and sedation - drowsiness may affect performance of skilled tasks (but sedation might actually be desirable in palliative care)
317
Q

Describe dopamine receptor antagonists (eg. domperidone and metoclopramide)

A
  • used for drug induced vomiting (eg cancer chemotherapy, treatment of parkinsons disease with agents stimulating dopaminergic transmission) and vomiting in GI disorders
  • use in children is restricted
  • complex mechanism of action (a lack of understanding of the source of dopamine to stimulate dopamine receptors in many circumstances)
  • centrally block dopamine D2 (and D3) receptors inn the CTZ
  • peripherally exert a prokinetic action on the oesophagus, stomach and intestine
  • domperidone does not cross the blood brain barrier and is less likely to result in the many unwanted effects of metoclopramide (eg. disorders of movement (extrapyramidal effects))
  • not effective against motion sickness
  • phenothiazines; which owe part of their action to dopamine D2 blockade - are used for severe nausea and vomiting
318
Q

Describe NK1 receptor antagonists (aprepitant)

A
  • used in combination with a 5-HT3 receptor antagonist and dexamethasone in the acute phase of highly emetogenic chemotherapy. in combination with dexamethasone in the delayed phase
  • exact site of action is uncertain, but antagonism of substance P (which causes vomiting and is released by vagal afferents) is assumed
319
Q

Describe cannabinoid (CB1) receptor agonists (nabilone)

A
  • used ideally in in-patient setting for treatment of cytotoxic chemotherapy this is unresponsive to other anti-emetics
  • decreases vomiting induced by agents stimulating the CTZ. evidence suggests that opiate receptors are involved in drug effect
  • numerous unwanted effects; drowsiness, dizziness, dry mouth, mood changes are common
320
Q

The portal vein carries outflow to where?

A
  • spleen
  • oesophagus
  • stomach
  • pancreas
  • small and large intestine
321
Q

Describe the portal system

A
  • superior mesenteric
  • splenic vein
  • gastric
  • part from inferior mesenteric
  • all combined create portal vein
322
Q

Describe hepatic blood flow

A
  • oxygenated blood from hepatic artery and nutrient rich, deoxygenated blood from hepatic portal vein
  • liver sinusoids
  • central vein
  • hepatic vein
  • inferior vena cava
  • right atrium of heart
323
Q

Describe portocaval anastomosis (portal vein collaterals)

A
  • the portal venous system has several anastomosis with the systemic venous system
  • four collateral pathways; oesophageal and gastric venous plexus
  • umbilical vein from the left portal vein to the epigastric venous system
  • retroperitoneal collateral vessels
  • the haemorrhoidal venous plexus
  • in cases of portal hypertension these anastomoses may become engorged, dilated or varicosed and subsequently rupture
324
Q

Describe portal hypertension (PH)

A
  • portal vein pressure above the normal range of 5 to 8 mmHg
  • portal vein; hepatic vein pressure gradient greater than 5mmHg
  • represents an increase of the hydrostatic pressure within the portal vein or its tributaries
325
Q

Describe causes of portal hypertensions classification according to site of obstruction

A
  • not just cirrhosis
  • prehepatic; blockage of the portal vein before the liver, due to portal vein thrombosis or occlusion secondary to congenital portal venous abnormalities
  • intrahepatic; due to distortion of the liver architecture either; presinusoidal (eg. schistosomiasis or non-cirrhotic portal hypertension), postsinusoidal (cirrhosis), budd chiari syndrome and veno-occlusive disease
326
Q

Portal hypertension results from both what?

A
  • increased resistance to portal flow

- increased portal venous return

327
Q

Describe signs of compensated cirrhosis

A
  • spider naevi
  • plamar erythema
  • clubbing
  • gynaecomastia
  • hepatomegaly
  • splenomegaly
  • or none
328
Q

Describe signs of decompensated cirrhosis

A
  • jaundice
  • ascites
  • encephalopathy
  • bruising
329
Q

Name complications of cirrhosis

A
  • ascites
  • encephalopathy
  • variceal bleeding
  • liver failure
330
Q

Describe the general principles of treatment of decompensated cirrhosis

A
  • remove or treat the underlying cause
  • look for and treat infection
  • the physiology is not normal
  • low threshold to switch to gluconeogenesis and lipolysis and catabolism
331
Q

Describe treatment of encephalopathy

A
  • look for cause; infection, metabolic, drugs, liver failure
  • treat it
  • lactulose to clear gut / reduce transit time; rifaximin
  • maintain nutritional status with small frequent meal / snack pattern and bedtime CHO
  • if spontaneous consider transplantation
332
Q

Describe acute effects of excess alcohol use

A
  • accidents
  • violence
  • oesophagitis, gastritis / ulceration
  • acute pancreatitis
  • overdose
  • aspiration
333
Q

Describe chronic effects of excess alcohol use

A
  • GI; stomach, liver, gallbladder
  • cardio; hypertension, cardiomyopathy, MI, stroke
  • CNS; neuropathies
    • cerebellar degeneration
  • dementia
  • Wernicke- korsakoffs syndrome
334
Q

Describe clinical features of haemangioma

A
  • the most common liver tumour
  • female > male
  • hypervascular tumour
  • usually single small
  • well demarcated capsule
  • usually asymptomatic
335
Q

Describe diagnosis and management of haemangioma

A
  • ultrasound; echogenic spot, well demarcated
  • ct; venous enhancement from periphery to centre
  • MRI; high intensity area
  • no need for FNA
  • no need for treatment
336
Q

Describe clinical features of focal nodular hyperplasia (FNH)

A
  • benign nodule formation of normal liver tissue
  • congenital vascular anomaly; associated with osler-weber-rendu and liver haemangioma
  • classically central scar containing a large artery, radiating branches to the periphery
  • hyperplastic response to abnormal arterial flow
  • sinusoids, bile ductules and Kupffer cells present on histology
  • more common in young and middle age women
  • no relation with sex hormones
  • usually asymptomatic, may cause minimal pain
337
Q

Describe diagnosis and management of focal nodular hyperplasia (FNH)

A
  • ultrasound; nodule with varying echogenicity
  • ct; hypervascular mass with central scar
  • MRI; iso or hypo intense
  • FNA; normal hepatocyte and Kupffer cells with central core
  • no treatment necessary
338
Q

Describe clinical features of hepatic adenoma

A
  • benign neoplasm composed of normal hepatocytes, no portal tract, central veins or bile ducts
  • more common in women
  • associated with contraceptive hormones and anabolic steroids
  • usually asymptomatic but may have RUQ pain
  • may present with rupture, haemorrhage or malignant transformation (very rare)
  • malignant transformation risk higher in males
339
Q

Describe the demographics of hepatic adenoma

A
  • most are solitary fat containing lesions
  • incidence is increasing
  • often found incidentally on imaging
  • usually in the right lobe
  • symptoms (pain, bleeding) are size related
  • multiple adenomas (adenomatosis) is a rare condition associated with glycogen storage diseases
340
Q

Describe hepatic adenoma and oral contraceptive / androgenic steroids

A
  • association is well documented, but no large epidemiologic studies to quantify risk
  • mechanism of hepatocyte transformation poorly understood identifiable oncogene mutations within adenomas that confer malignant risk
  • risk of adenomas related to duration of OC use (>2 years) and oestrogen component, but adenomas have been described with even 6 month of OC use
  • regression can occur after discontinuation
341
Q

Describe diagnosis and management of hepatic adenomas

A
  • ultrasound; filling defect
  • CT; diffuse arterial enhancement
  • MRI; hypo or hyper intense lesion
  • FNA; may be needed
  • stop hormones, weight loss
  • males (irrespective of size); surgical incision
  • females; imaging after 6 months
342
Q

Describe adenomas in young patients

A
  • hypervascular
  • purely a hepatocyte tumour, cold on nuclear sulfur colloid scan
  • may cause pain and can bleed
  • malignant degeneration
343
Q

Describe focal nodular hyperplasia in young patients

A
  • hypervascular
  • contains all the liver ultrastructure including RES and bile ductules (isointense on sulfur colloid scan)
  • may cause pain
  • central scar
  • no malignant risk
  • minimal bleeding risk
344
Q

Name types of cystic lesions

A
  • simple
  • hydatid
  • atypical
  • polycystic lesion
  • pyogenic or amoebic abscess
345
Q

Describe clinical features of a simple cyst

A
  • liquid collection lined by an epithelium
  • no biliary tree communication
  • most of the time asymptomatic
  • solitary and uniloculated
  • symptoms can be related to intracystic haemorrhage, infection, rupture (rare), compression
346
Q

Describe management of a simple cyst

A
  • no follow up necessary
  • if doubt, imaging in 3-6 months
  • if symptomatic or uncertain diagnosis (complex cystic lesion), then consider surgical intervention
347
Q

Describe clinical features of hydatid cyst

A
  • enchinoccocus granulosus
  • endemic regions; eastern Europe, central America and south America, middle east and north America
  • patients may present with disseminated disease, or erosion of cysts into adjacent structure and vessels (IVC)
  • clinical diagnosis based on history, appearance and serologic testing detection of anti-echinococcus antibodies
348
Q

Describe management of a hydatid cyst

A
  • surgery
  • conservative; open cystectomy, marsupialization
  • radical; pericystectomy, lobectomy
  • risks; operative morbidity, anaphylaxis, dissemination of infection
  • medical; albendazole
  • percutaneous drainage; PAIR
349
Q

Describe polycystic liver disease (PLD)

A
  • embryonic ductal plate malformation of the intrahepatic biliary tree
  • numerous cysts throughout liver parenchyma
  • three types; von meyenburg complexes (VMC), polycycstic liver disease, autosomal dominant polycystic kidney disease
350
Q

Describe von meyenburg complexes (VMC)

A
  • von meyenburg complexes (microhamartomas) benign cystic nodules throughout the liver
  • cystic bile duct malformations, originating from the peripheral biliary tree
  • remnants develop into small hepatic cysts and usually remain silent during life
  • not germline genetically driven
  • incidental finding
351
Q

Describe management of polycystic liver disease

A
  • C/O abdominal pain, abdominal distension, atypical symptoms due to voluminous cysts resulting in compression of adjacent tissue or failure of the affected organ
  • conservative treatment is recommended to halt cyst growth to allow abdominal decompression and ameliorate symptoms
  • invasive procedures are rarely required only in selective patient group with advanced PCLD, ADKPD or liver failure, defenestration / aspiration, liver transplantation
  • pharmacological therapy by somatostatin analogues lead to beneficial outcome of PLD in terms of symptom relief and liver volume reduction
352
Q

Describe clinical features of a liver abscess

A
  • high fever
  • leucocytosis
  • abdominal pain
  • complex liver lesion
  • history of abdominal or biliary infection, dental procedures
353
Q

Describe management of liver abscesses

A
  • initial empiric broad spectrum antibiotics
  • aspiration / drainage percutaneously
  • echocardiogram
  • operation if no clinical improvement; open drainage, resection
  • 4 weeks antibiotic therapy with repeat imaging
354
Q

Name malignant liver tumours

A
  • hepatocellular carcinoma (HCC)
  • fibro-lamellar carcinoma of the liver
  • hepatoblastoma
  • intrahepatic cholangiocarcinoma
  • others
  • metastases
355
Q

Name risk factors for hepatocellular carcinoma

A
  • most important risk factor is cirrhosis from any cause
  • hepatitis B (integrates in DNA)
  • hepatitis C
  • alcohol
  • aflatoxin
  • other
356
Q

Describe clinical features of hepatocellular carcinoma

A
  • weight loss and RUQ pain (most common)
  • asymptomatic
  • worsening of pre-existing chronic liver disease
  • acute liver failure
  • signs of cirrhosis
  • hard enlarged RUQ mass
  • liver bruit (rare)
357
Q

Describe metastases of hepatocellular carcinoma

A
  • rest of the liver
  • portal vein
  • lymph nodes
  • lung
  • bone
  • brain
358
Q

Describe labs for hepatocellular carcinoma

A
  • labs of liver cirrhosis
  • AFP (alfa fetoprotein)
  • is an HCC tumour marker
  • values >100ng/ml highly suggestive of HCC
  • elevation seen in 60-80% of patients
  • AFP sensitivity of 41-65% and specificity of 80-94% when the cut off value is 20ng/L
359
Q

Diagnosis of hepatocellular carcinoma

A
  • clinical presentation
  • elevated AFP
  • US
  • triphasic CT scan; very early arterial perfusion
  • MRI
  • biopsy
360
Q

Describe prognosis of hepatocellular carcinoma

A
  • tumour size
  • extrahepatic spread
  • underlying liver disease
  • pt performance status
361
Q

Describe fibro-lamellar carcinoma

A
  • presents in young patient (5-35)
  • not related to cirrhosis
  • AFP is normal
  • CT shows typical stellate scar with radial septa showing persistent enhancement
  • surgical resection or transplantation is the standard of care for fibrolamellar carcinoma
  • TACE for patients with unresectable tumour
362
Q

Describe secondary liver metastases

A
  • the most common site for blood born metastases
  • common primaries; colon, breast, lung, stomach, pancreas and melanoma
  • mild cholestatic picture (ALP) with preserved liver function
  • Dx imaging or FNA
  • treatment depends on the primary cancer
  • in some cases resection or chemoembolization is possible
363
Q

Describe functions of the pancreas

A
  • exocrine function; acinar cells secrete pancreatic enzymes
  • endocrine function; islets of Langerhans secrete hormones into blood
364
Q

Describe islets of Langerhans

A
  • beta cells ; secrete insulin
  • alpha cells; which secrete glucagon
  • delta cells; secrete somatostatin
  • F cells; secrete pancreatic polypeptide
365
Q

Describe pancreatic fluid

A
  • secretions regulated by vagus nerve and gastrin levels
  • secretions from the acinar cells
  • protease; trypsin and chymotrypsin, polypeptides to peptides
  • pancreatic lipase; triglycerides into fatty acids and monoglycerides
  • pancreatic amylase; carbohydrates into disaccharides / monosaccharides
  • other enzymes; ribonuclease, deoxyribonuclease, gelatinase and elastase
  • secretion from epithelial cells lining the ducts; bicarbonate, base that is critical to neutralise acidic gastric juice, water
366
Q

Define pancreatitis

A
  • an acute inflammation process in the pancreas, involves more regional tissues and remote organs
  • common cause for acute hospital admissions
  • incidence is rising
  • 80% of cases are managed with only analgesia and IV fluids
367
Q

Describe aetiology of pancreatitis

A
  • idiopathic
  • gallstones
  • ethanol
  • trauma
  • steroids
  • mumps (other infections coxsackie B and viral hepatitis)
  • autoimmune (IgG4 related disease, polyarteritis nodose)
  • scorpion bite
  • hypercalcaemia, hyperparathyroidism, hyperlipidaemia
  • ERCP
  • drugs (azathoprin)
368
Q

Describe symptoms of pancreatitis

A
  • acute onset epigastric pain
  • radiating through to back
  • very severe
  • double over
  • nausea and vomiting
  • jaundice
  • a trigger identified, eg. ERCP, gallstones, ETOH
369
Q

Describe examination findings of pancreatitis

A
  • diffuse upper abdominal tenderness
  • soft
  • normal BS
  • fullness in epigastrium, pseudocyst
  • if severe; can present like peritonitis with widespread guarding and absent BS
370
Q

Name classic signs of pancreatitis

A
  • erythema abigne
  • cullens sign
  • grey turners sign
371
Q

Describe initial investigations for pancreatitis

A
  • IV access
  • bloods; haematology; FBC and coagulation, biochem; u and es, LFTs, calcium, glucose, amylase / lipase, CRP and lactate
  • arterial blood gas; hypoxia, ARDS
372
Q

Describe CT scanning and pancreatitis

A
  • to assess severity of pancreatitis, day 5 from onset of symptoms
  • as follow up
  • for potential intervention
  • to look for complications; fluid collections, pancreatic / peripancreatic necrosis, ascites, bleeding, abscess
373
Q

Describe complications of pancreatitis

A
  • fluid collection
  • pseudocysts
  • abscess
  • necrosis +/- infection
  • ascites
  • pleural effusion
  • pulmonary failure
  • renal failure
  • shock
  • sepsis
  • metabolic acidosis
  • hyperglycaemia
  • hypocalcaemia
  • MODS
374
Q

Describe principles of management of pancreatitis

A
  • conservative in the first instance
  • fluid resuscitation
  • correct electrolytes
  • careful fluid balance
  • oxygen
  • antibiotics
  • nutrition
  • index admission laparoscopic cholecystectomy
375
Q

Describe pancreatic pseudocysts

A
  • complication of acute and chronic pancreatitis; due to +/- PD communication, can cause biliary obstruction, gastric outlet obstruction
  • diagnosis; pain, nausea, vomiting, jaundice, weight loss
  • treatment; nothing, endoscopic drainage
376
Q

Describe pancreatic pseudocysts

A
  • complication of acute and chronic pancreatitis
  • due to +/- PD communication
  • can cause biliary obstruction, gastric outlet obstruction
  • diagnosis; pain, nausea, vomiting, jaundice, weight loss
  • treatment; nothing, endoscopic drainage, radiological drainage, surgical drainage
377
Q

Describe pancreatic abscesses

A
  • abscess drained to control sepsis

- CT/US guided retroperitoneal or trans-peritoneal drainage

378
Q

Describe pancreatic necrosis

A
  • CT for assessment
  • sterile or infected
  • FNA for micro
  • percutaneous drain
  • open vs minimal invasive
  • necrosectomy and lavage
379
Q

Describe chronic pancreatitis

A
  • progressive and irreversible damage
  • loss of exocrine +/- endocrine function
  • presentation; very similar to acute pancreatitis, alcohol Hx; smokers, medications etc, masses / ascites / jaundice on examination
  • imaging; CXR/ASR, USS, CT pancreas, MRI, ERCP
380
Q

Describe aetiology of chronic pancreatitis

A
  • alcohol
  • idiopathic
  • PD obstruction
  • autoimmune
  • tropical countries
  • hereditary
381
Q

Describe management of chronic pancreatitis

A
  • manage any acute episodes appropriately
  • creon as enzyme replacement therapy if pancreatic insufficiency; bloating, pain, loose, fatty pale stools, weight loss, increase stool frequency
  • surgical options
382
Q

Describe complications of chronic pancreatitis

A
  • splenic vein thrombosis
  • pseudoaneurysm - splenic artery
  • pleural effusions
  • ascites
  • pancreatic cancer
  • pseudocysts
383
Q

Describe pseudocysts

A
  • 25-30% with PD communication
  • biliary obstruction
  • gastric outlet obstruction
  • management; endoscopic drainage, surgical drainage, resection
384
Q

Describe complications of pseudocysts

A
  • splenic vein thrombosis
  • pseudoaneurysm; splenic artery
  • pleural effusions
  • ascites
  • pancreatic cancer
  • biliary obstruction
  • duodenal obstruction
385
Q

Describe duodenal obstruction

A
  • oedema due to acute flare up
  • fibrosis and pancreatic head tumour
  • pseudocyst
  • management; stent, bypass, resection
386
Q

Name types of pancreatic tumour

A
  • exocrine; adenocarcinoma

- endocrine; gastrinoma, insulinoma, glucagonoma

387
Q

Describe symptoms of pancreatic tumours

A
  • jaundice (painless)
  • loose pale stools
  • dark urine
  • weight loss
  • back pain
388
Q

Describe gallstones

A
  • common
  • most asymptomatic
  • colic, cholecystitis, jaundice, pancreatitis, bowel obstruction
389
Q

Describe risk factors of gallstones

A
  • age >40
  • female
  • high fat diet
  • obesity
  • pregnancy
  • hyperlipidaemia
  • bile salt loss (crohns)
  • diabetes
  • dysmotility of GB
  • prolonged fasting
  • TPN
390
Q

Why do we get gallstones?

A
  • abnormal bile composition
  • bile stasis
  • infection
  • excess cholesterol
  • excess bilirubin
391
Q

Describe categories of gallstones

A
  • mixed
  • cholesterol
  • pigment
  • primary bile duct stones (rare)
392
Q

Describe biliary colic

A
  • stone impacts in cystic duct
  • gradual build-up pain in RUQ
  • radiates to back / shoulder
  • may last 2-6 hours
  • associated with indigestion / nausea
393
Q

Describe severe acute epigastric pain

A
  • biliary colic
  • peptic ulcer disease
  • oesophageal spasm
  • myocardial infarction
  • acute pancreatitis
394
Q

Describe diagnosis of gallstones

A
  • ultrasound
  • CT scan
  • MRCP / ERCP
  • HIDA
  • EUS
395
Q

Describe treatment of biliary colic

A
  • pain killers
  • low fat diet / lose weight if obese
  • observe 3-6 months
  • recurrent episodes pain / colic
  • consider / refer for surgery
  • cholecystectomy
  • unfit; ursodeoxycholic acid 10mg/kg/day
396
Q

Describe acute cholecystitis

A
  • inflammation in GB, obstruction of cystic duct

- initially sterile, then becomes infected

397
Q

Treatment of acute cholecystitis

A
  • IV antibiotics and IV fluids
  • nil by mouth
  • US to confirm diagnosis
  • urgent cholecystectomy ASAP
  • interval cholecystectomy
398
Q

Describe complications of gallstones

A
  • stone may migrate into CBD; jaundice, cholangitis, acute pancreatitis
  • gallstone ileus
399
Q

Describe diagnosis of CBD pathology

A
  • itch, nausea, anorexia
  • jaundice
  • abnormal LFTs
  • ERCP; ES and stone removal
  • surgical exploration; CBD (open vs lap)
400
Q

Describe gallstone ileus

A
  • small bowel obstruction
  • fistula gallbladder + duodenum
  • large gallstone passes into small intestine
  • move down SB causing intermittent colic
  • present with distal SB obstruction
401
Q

Describe treatment of gallstone ileus

A
  • urgent laparotomy; SB enterotomy to remove stone

- interval cholecystectomy in 3 months

402
Q

Name the best single test for gallstones

A
  • ultrasonography
403
Q

Describe cholangiocarcinoma

A
  • second most common hepatobiliary cancer

- increased incidence in UK since mid 1990s

404
Q

Describe clinical presentation and staging / assessment of cholangiocarcinoma

A
  • usually presents late
  • jaundice, weight loss, anorexia, lethargy
  • duplex ultrasound
  • spiral CT, ERCP, PTC
  • MRI, MRCP, MRA
405
Q

Describe visceral pain

A
  • receptors are located on the serosal surface, in the mesentery, within the intestinal muscle and mucosa of the hollow organ
  • these pain receptors respond to mechanical and chemical stimuli, such as stretching, tension and ischaemia
  • because visceral pain fibres are c fibres, pain is often dull, poorly localised and perceived in the middle
  • there are 3 broad pain areas with anatomic association; foregut felt in the middle (stomach, pancreas)
  • midgut felt in suprapubic (small intestine)
  • hindgut felt in lower abdomen (colon)
406
Q

Describe somato-parietal pain

A
  • the receptors are located in the parietal peritoneum, the muscle and the skin
  • the pain resulting from; inflammation, stretching or tearing of the parietal peritoneum
  • it is transmitted through mialinated A, delta to specific dorsal root ganglia
  • this pain is characterised by sharp, more intense and more localised sensation
  • movement may aggravate pain so patient very often lay still
407
Q

Describe referred pain

A
  • it is well localised but felt in distant areas of the cutaneous dermatome as the effected organ
  • it occurs when organs share common nerve pathways
  • for example; gall bladder pain may be felt in the right should tip
408
Q

Define the acute abdomen

A
  • refers to a sudden, severe abdominal pain, that is less than 24 hours of duration
409
Q

Name causes of acute abdomen

A
  • acute appendicitis
  • acute pancreatitis
  • acute peptic ulcer
  • acute diverticulitis
  • diabetic ketoacidosis
  • bowel perforation
  • volvulus
  • acute pyelonephritis
  • acute cholecystitis
  • acute intestinal ischaemia
  • acute renal colic
  • leaking AAA
  • peritonitis
  • strangulated hernia
410
Q

Name vital signs of acute abdomen

A
  • is patient hypotensive, tachycardic, haemodynamically unstable
  • MI, AAA, ruptured ectopic, mesenteric ischaemia, rupture spleen liver, septic, dehydrated
411
Q

Describe an abdominal mass

A
  • abnormal growth in the abdomen
  • an abdominal mass causes visible swelling and may change the shape of the abdomen
  • masses in the abdomen are often described by their location
  • or by the origin of the mass; fat, faeces, flatus, foetus, fluid or fatal growth
412
Q

What is a hernia?

A

An abnormal protrusion of a cavitys contents through a weakness in the wall of the cavity

413
Q

Describe causes of abdominal hernias

A
  • anatomical eg. sites where structure exit through and opening in the cavity
  • inherited collagen disorders
  • sites where surgical incisions are made
414
Q

Name types of abdominal hernias

A
  • epigastric
  • umbilical / paraumbilical
  • inguinal hernia
  • femoral hernia
  • Spigelian hernia
  • lumbar hernia
  • incisional hernia
  • parastomal hernia
  • port-site hernia
415
Q

Describe classification of hernias

A
  • reducible; hernia can be easily pushed back into the abdomen
  • incarcerated or irreducible hernia; when a hernia cannot be manipulated back to the abdomen
  • strangulated hernia; vascular supply to the contents contained within the hernia is compromised, resulting in ischaemic and gangrenous tissue
416
Q

Describe treatment of hernias

A
  • conservative / non-surgical management

- surgical management

417
Q

Describe epigastric hernias

A
  • is defined as a fascial defect in the linea alba between the xiphoid process and the umbilicus
  • main presentation is a midline lump
  • asymptomatic (75%) or can present with pain
  • if incarcerated or strangulated symptoms depend on organ involved
  • management is either conservative or surgical
418
Q

Describe paraumbilical hernias

A
  • acquired hernias occur in all age groups
  • aetiological factors include stretching of the abdominal wall by obesity, multiple pregnancy and ascites
  • frequently symptomatic presenting with pain
  • para-umbilical hernias do not resolve spontaneously and have a high incidence of incarceration and strangulation
  • management nearly always surgical
419
Q

Describe adult umbilical hernias

A
  • usually results from persistent elevation of intraabdominal pressure
  • the clinical presentation, management and complications of adult umbilical hernia are very similar to those of para-umbilical hernia
420
Q

Describe the anatomy of the inguinal canal

A
  • 4cm in length, starts at deep inguinal ring and ends in superficial inguinal ring
  • boundaries; anterior - external oblique aponeurosis, floor - ligament, roof - conjoint tendon, posterior - transversalis fascia
  • transmits the spermatic cord and ilioinguinal nerve in the males and the round ligament of the uterus and ilioinguinal nerve in the female
421
Q

Describe the contents of the spermatic cord

A
  • three coverings; internal spermatic fascia, cremasteric fascia, external spermatic fascia
  • six contents; vas deferens, pampiniform plexus (veins), lymphatics, remain of the processus vaginalis, nerves; genital branch of genitofemoral nerve and sympathetic twigs, 3 arteries; testicular artery, artery to the vas and cremasteric artery
422
Q

Describe the hesselbach triangle

A
  • laterally; inferior epigastric artery
  • medially; lateral border of the rectus muscle
  • inferiorly; inguinal ligament
423
Q

Name types of inguinal hernia

A
  • indirect inguinal hernia

- direct inguinal hernia

424
Q

Describe diagnosis of inguinal hernia

A
  • groin swelling which usually disappears when lying down
  • usually located above and medial to the pubic tubercle
  • palpable cough impulse on examination
  • if in doubt dynamic ultrasound scan can be helpful
425
Q

Describe management of inguinal hernia

A
  • non surgical

- surgical ; open, laparoscopic

426
Q

Describe the anatomy of the femoral ring

A
  • anteriorly; inguinal ligament
  • posteriorly; iliopectineal ligament
  • medially; lacunar ligament
  • laterally; femoral vein
427
Q

Describe an incisional hernia

A
  • iatrogenic

- commonest complication of a laparotomy (exploration of the abdomen)

428
Q

Describe haemorrhoids

A
  • enlarged vascular cushions in the lower rectum and anal canal
  • at least 10% of the population have symptomatic haemorrhoids at some time in their life
429
Q

Describe the presentation of haemorrhoids

A
  • painless bleeding
  • fresh, bright red blood, not mixed with stool, usually on the paper
  • perianal itchiness
  • no change in bowel habit, no weight loss or other associated symptoms
430
Q

Describe clinical findings of haemorrhoids

A
  • external inspection can be normal
  • maceration of the perianal skin
  • obvious haemorrhoids if 3rd degree piles presents
  • DRE - normal unless thrombosed
431
Q

Describe the classical position of haemorrhoids

A
  • corresponds to the branches of the superior haemorrhoidal artery occurring at 3,7 and 11 o’clock position with the patient in the lithotomy position
432
Q

Describe investigations of haemorrhoids

A
  • PR exam
  • rigid sigmoidoscopy
  • proctoscopy
  • flexible sigmoidoscopy if patients is above 50
433
Q

Describe treatment of haemorrhoids

A
  • symptomatic
  • sclerosation therapy with 5% phenol in almond oil
  • rubber band ligation
  • open haemorrhoidectomy
  • stapled haemorrhoidectomy
  • HALO / THD procedure
434
Q

Describe the HALO/THD procedure

A
  • haemorrhoidal artery ligation
  • devised by Japanese surgeons in 1995
  • the operation is best performed under general or spinal anaesthesia
435
Q

Describe the HALO procedure

A
  • miniature doppler ultrasound device locates branches of arteries supplying the haemorrhoids
  • these blood vessels are tied off, and the haemorrhoid shrinks over the subsequent days and weeks
  • because the stitch is placed in the lower rectum where there are virtually no sensory nerves the procedure is pain free
436
Q

Name the types of rectal prolapse

A
  • partial (anterior mucosal prolapse)

- complete (full thickness)

437
Q

Describe the presentation of rectal prolapse

A
  • protruding mass from anus especially during defecation
  • may reduce spontaneously
  • bleeding and passing mucus per rectum is common
  • examination usually shows poor anal tone
438
Q

Describe management of complete rectal prolapse

A
  • many patients too frail for surgery - bulking agent and education on manual reduction
  • delormes procedure
  • perineal rectopexy
  • abdominal rectopexy
  • anterior resection
439
Q

Describe management of incomplete prolapse

A
  • in children; dietary advice and treatment of constipation

- in adults; treatment similar to that of haemorrhoids

440
Q

Describe anal fissures

A
  • tear in the anal margin due to passage of a constipated stool
  • usually in the midline posteriorly but may be occasionally anterior
  • multiple fissures may be due to crohns disease
441
Q

Describe the presentation of anal fissures

A
  • acute onset of severe anal pain usually following episode of constipation
  • ‘glass passing through the back passage’
  • pain lasts for up to 1/2 hr after defecation
  • bright rectal bleeding
442
Q

Describe treatment of anal fissures

A
  • dietary advice, stool softeners
  • pharmacological sphincterotomy (GTN ointment, diltiazem ointment) PR for 6/52
  • lateral sphincterotomy
  • botox injection
443
Q

Describe fistula in ano

A
  • abnormal communication between two epithelial surfaces
  • there is an internal opening in the anal canal and one or more external openings on the peri-anal skin
  • also rarely caused by crohns disease, TB and carcinoma
444
Q

Describe the presentation of fistula in ano

A
  • majority arise from delay in treatment or inadequate treatment of anorectal abscess
  • could have crohns disease, carcinoma or TB as an underlying pathology
445
Q

Describe investigations of fistula in ano

A
  • EUA of anorectum
  • rigid sigmoidoscopy, proctoscopy
  • flexible sigmoidoscopy
  • MRI
446
Q

Describe management of fistula in ano

A
  • laying open
  • two stage procedure
  • insertion of seton (draining, cutting)
  • LIFT procedure
  • glue / Permacol
  • defunctioning colostomy
447
Q

Describe complications of fistula in ano

A
  • pain
  • bleeding
  • incontinence of flatus or stool
  • recurrence
  • further surgery
448
Q

Describe cardiovascular surgery complications

A
  • haemorrhage
  • MI
  • DVT
449
Q

Describe the presentation of haemorrhage

A
  • overt
  • tachycardia
  • hypotension
  • oliguria
450
Q

Describe prevention of haemorrhage

A
  • meticulous technique
  • avoidance of sepsis
  • correction of coagulation disorders
451
Q

Describe prevention of MI

A
  • delay surgery after MI
  • avoidance of perioperative hypotension
  • correction of ischaemic heart disease
452
Q

Name respiratory surgical complications

A
  • atelectasis
  • pneumonia
  • PE
453
Q

Describe atelectasis / pneumonia

A
  • collapse of lung tissue&raquo_space; infection
  • anaesthesia; increases secretion, inhibits cilia
  • postoperative pain; inhibits coughing
  • aspiration; stomach contents
454
Q

Describe GI surgical complications

A
  • ileus
  • anastomotic dehiscence
  • ashesions
455
Q

Describe ileus

A
  • paralysis of intestinal motility
  • caused by; handling of bowel
  • peritonitis
  • retroperitoneal injury
  • immobilisation
  • hypokalaemia
  • drugs
456
Q

Describe presentation of ileus

A
  • vomiting
  • abdominal distension
  • dehydration
  • silent abdomen
457
Q

Describe the prevention of ileus

A
  • minimal operative trauma
  • laparoscopy
  • avoidance of intra-abdominal sepsis
458
Q

Describe anastomotic dehiscence

A
  • breakdown of anastomosis; intestinal, vascular, urological
  • caused by; poor technique, poor blood supply, tension on anastomosis
459
Q

Describe the presentation anastomotic dehiscence

A
  • intestinal; peritonitis, abscess, ileus, fistula
  • vascular; bleeding / haematoma
  • urological; leakage of urine / urinoma
460
Q

Describe adhesions

A
  • fibrin to fibrous tissue; bowel to bowel, bowel to abdominal wall and other structures, lung to chest wall
  • caused by; inflammatory response, ischaemia
461
Q

Describe the presentation of adhesions

A
  • asymptomatic; to chest wall

- intestinal obstruction; vomiting, pain, distension, constipation

462
Q

Describe the presentation of wound infection

A
  • pyrexia (5-8 days)
  • redness
  • pain
  • swelling
  • discharge
463
Q

Describe the prevention of wound infection

A
  • pre-op preparation
  • skin cleansing
  • aseptic technique
  • avoidance of contamination
  • prophylactic antibiotics
464
Q

Describe urinary complications of surgery

A
  • acute retention of urine
  • urinary tract infection
  • urethral stricture
  • acute renal failure
465
Q

Describe neurological complications of surgery

A
  • confusion
  • stroke
  • peripheral nerve lesions; ulnar nerve, radial nerve, sciatic nerve, common peroneal nerve
466
Q

Describe causes of confusion

A
  • hypoxia; chest infections, PE, MI
  • oversedation
  • sepsis
  • electrolyte imbalance
  • stroke
  • hyper or hypoglycaemia
  • alcohol or tranquiliser withdrawal
467
Q

Describe the presentation of confusion

A
  • disorientation; time, place
  • paranoia
  • hallucinations
468
Q

Describe how to minimise complications and their effect

A
  • patient selection and preparation
  • careful surgery
  • constant vigilance
469
Q

Describe the unique blood supply to the liver

A
  • blood flow out of the liver through 3 hepatic veins into a big vein called the IVC
  • oxygen rich blood flows into the liver through the hepatic artery
  • nutrient rich blood coming from the bowel flows into the liver through the portal vein
  • bile flows out of the liver through the bile duct
470
Q

Name functions of the liver

A
  • protein metabolism
  • carbohydrate metabolism
  • lipid metabolism
  • bile acid metabolism
  • bilirubin metabolism
  • hormone and drug metabolism
  • immunological defence
471
Q

Describe acute liver disease

A
  • any insult to the liver causing damage in previously normal liver
  • less than 6 months duration
  • acute liver failure defined as causing encephalopathy and prolonged coagulation
  • wilsons disease may allow classification od an acute presentation as acute liver failure
472
Q

Describe clinical features of acute liver disease

A
  • none
  • jaundice
  • lethargy
  • nausea
  • anorexia
  • pain
  • itch
  • arthralgia
  • abnormal LFTs
473
Q

Describe causes of acute liver disease

A
  • viral A,B,C,D,E,CMV,EBC and toxoplasmosis
  • drugs
  • shock liver
  • cholangitis
  • alcohol
  • malignancy
  • chronic liver disease
  • ask about paracetamol
  • rare; budd chiari, acute fatty liver of pregnancy, cholestasis of pregnancy
474
Q

Describe investigations of acute liver disease

A
  • LFTs (including albumin and bilirubin)
  • prothrombin time
  • history and examination
  • ultra sound including vascular
  • virology
  • investigations of chronic liver disease
  • rarely liver biopsy
475
Q

Describe the treatment of acute liver disease

A
  • rest, up to 3 months for recovery, may be 6 months
  • fluids, no alcohol
  • increase calories, high fat food poorly tolerated
  • for itch; sodium bicarbonate bath, cholestyramine or ursodeoxycholic acid
  • observation for fulminant hepatic failure
476
Q

Describe hepatic drug reactions

A
  • 6 weeks exposure to effect; first effect may not have been noticed, liver may not have been normal to start
  • any drug
  • multiple mechanisms; therefore multiple patterns of LFTs and symptoms, may overlap with other toxic effects
477
Q

Describe fulminant hepatic failure (FHF)

A
  • acute episode of severe liver dysfunction (jaundice and encephalopathy) in a patient with a previous normal liver
478
Q

Describe causes for FHF

A
  • common; paracetamol, fulminant viral, drugs, HBV, non A-E

- rare; AFLP, mushrooms, malignancy, wilsons, budd chiari, HAV

479
Q

Describe FHF clinical cause and complications

A
  • encephalopathy
  • hypoglycaemia
  • coagulopathy
  • circulatory failure
  • renal failure
  • infection
480
Q

Describe FHF assessment

A
  • exclude cirrhosis, alcohol induced injury or malignant infiltration
  • initiate early discussion with tertiary liver / transplant centre, even if not immediately relevant
  • screen intensively for hepatic encephalopathy
  • determine aetiology
  • to guide treatment and determine prognosis
  • assess suitability for liver transplant
  • contraindications should not preclude transfer to tertiary liver / transplant centre
  • if the patient has an INR >1.5 and onset of hepatic encephalopathy or other poor prognostic features
481
Q

Describe FHF treatment

A
  • supportive
  • inotropes and fluids
  • renal replacement
  • management of raised ICP
  • transplantation
482
Q

Name the first line investigation of cholecystitis / biliary colic

A

Ultrasound

483
Q

Describe pancreatitis and imaging

A
  • main purpose of imaging is to evaluate complications
  • necrosis
  • intra-abdominal collections
  • vascular complications
  • best performed around 1 week following onset of symptoms
484
Q

Name the first line investigation of perforation

A

Erect CXR

485
Q

Name the first line investigation for appendicitis

A
  • ultrasound
486
Q

Name the investigation for diverticulitis

A

CT

487
Q

Describe chronic liver disease

A
  • duration greater than 6 months
  • can present acutely
  • duration may be sub clinical
  • outcome; progression to cirrhosis
  • signs and symptoms dependent on underlying disease or features of cirrhosis
  • pathology recurrent inflammation and repair with fibrosis and regeneration
488
Q

Name causes of chronic liver disease; cirrhosis causes

A
  • alcohol
  • NAFLD
  • hepatitis C
  • primary biliary cholangitis
  • autoimmune hepatitis
  • hepatitis B
  • haemochromatosis
  • primary sclerosing cholangitis
  • wilsons disease
  • alpha 1 anti-trypsin
  • budd-chiari
  • methotrexate
489
Q

Describe NAFLD

A
  • commonest disease in the world
  • 20-30% of general population have fatty liver
  • 20-30% will have NASH
  • of these 20% will have cirrhosis within 20 years
  • in obesity rate up to 60^
  • a spectrum
  • steatosis
  • NASH (fibrosis)
490
Q

Describe histological features of NASH

A
  • spectrum; steatosis > steatohepatitis > steatohepatitis with fibrosis > cirrhosis
  • steatohepatitis; inflammation usually mild, lobular, and mixed mononuclear and neutrophilic
  • hepatocyte degeneration; ballooning and Mallory bodies
  • fibrosis; initially pericellular, later bridging
  • cirrhosis; occurs in up to 20£ over 10 years
491
Q

Describe the aetiology of primary biliary cholangitis

A
  • first described 1851 gull and Addison
  • autoimmune component 1960s, 1970s - 1980s AMAs M1-M12
  • 1980s target ME-E2 E3 subunits of PDC-E2 n inner leaflet of mitochondrial membrane
  • t-cell mediated, CD4 cells reactive to M2 target, why loss of tolerance
492
Q

Describe the presentation of primary biliary cholangitis

A
  • middle aged women (f:m 10:1)
  • usually asymptomatic / incidental
  • symptoms; fatigue, itch without rash, xanthesalma, xanthomas
  • complications
493
Q

Describe primary biliary cholangitis diagnosis and treatment

A
  • 2 of 3; positive AMA, cholestatic LFTs, liver biopsy

- treatment; ursodeoxycholic acid, obeticholic acid

494
Q

Describe PBC outcomes

A
  • most will not develop symptoms in their life time
  • the majority with PBC symptoms do not develop liver failure; itch can be particularly problematic
  • many developing liver failure will be unfit for transplant
  • still a common cause of liver transplantation
495
Q

Describe auto-immune hepatitis type one and type 2 immunology

A
  • type 1; adult (twin peaks), ANA, ASMA 1 in 40 actin, SLA severity, uncommon
  • type 2; children and young adults, LKM1, exclusive, AMA, very rare
496
Q

Describe type 1 auto-immune hepatitis

A
  • bimodal age distribution (ages 10-20 and 45-70)
  • female: male 3.6:1
  • associated with extrahepatic manifestations: autoimmune thyroiditis, graves disease, chronic UC. Les commonly with RA, pernicious anaemia, systemic sclerosis, ITP, SLE
  • 40% present with acute onset of symptoms similar to toxic hepatitis or acute viral hepatitis
497
Q

Describe the clinical presentation of type 1 auto-immune hepatitis

A
  • hepatomegaly
  • jaundice
  • stigmata of chronic liver disease
  • splenomegaly
  • elevated AST and ALT
  • elevated PT
  • non-specific symptoms; malaise, fatigue, lethargy, nausea, abdominal pain, anorexia
498
Q

Describe diagnosis of type 1 auto-immune hepatitis

A
  • elevated AST and ALT
  • elevated IgG
  • rule out other causes; wilsons disease, alpha 1 antitrypsin deficiency, viral hepatitis (A,B,C), drug induced liver disease (alcohol, minocycline, nitrofurantoin, INH, PTU, methyldopa etc)
  • presence of autoimmune antibodies
  • liver biopsy
499
Q

Describe the pathogenesis of type 1 auto-immune hepatitis -

A
  • unknown mechanism but several proposed mechanisms
  • genetically predisposed individual with exposure to an environmental agent triggers the autoimmune pathogenic process
  • genetic predisposing factors; HLA-DR3; early onset, severe form
  • HLA-DR4; Caucasian, late onset, better response to steroids, higher incidence of extrahepatic manifestations
  • IgG; part of the IgG molecule (mainly the heavy chain)
  • t cell receptors
500
Q

Describe the treatment of type 1 autoimmune hepatitis

A
  • corticosteroids
  • azathioprine
  • children: azathioprine or 6MP, combination therapy
  • prednisolone and azathioprine
  • prednisolone; start AT 30MG daily and taper down to 15mg at week 4, then maintain on 5mg daily until therapy endpoint
  • azathioprine 50-100mg daily
501
Q

Describe the prognosis of autoimmune hepatitis

A
  • 40% of all patients with AIH develop cirrhosis
  • 54% develop oesophageal varices within 2 years
  • poor prognosis if has presence of ascites or hepatic encephalopathy
  • 13-20% of patients can have spontaneous resolution
  • of patients who survive the most early and active stage of disease, approximately 41% of them develop inactive cirrhosis
  • of patients who have severe initial disease and survive the first 2 years, typically survive long term
502
Q

Describe primary sclerosing cholangitis

A
  • autoimmune destructive disease of large and medium sized bile ducts
  • commonest liver disease in scandanavia
  • clinical recurrent cholangitis
  • diagnosis imaging of biliary tree
  • treatment maintain bile flow, monitor for cholangiocarcinoma and colo-rectal cancer
503
Q

Describe haemochromatosis

A
  • genetic iron overload syndrome
  • mono-genetic autosomal recessive disease of iron overload, C282Y or H63D, mutations in HFE gene
  • gene carrier frequency 10%, genetic haemochromatosis 1 in 200 but partial penetrance
  • cirrhosis, cardiomyopathy, pancreatic failure, the bronzed diabetic
  • treatment = venesection
504
Q

Describe Wilsons disease

A
  • lenticulo-hepatic degeneration
  • mono-genetic autosomal recessive disease
  • loss of function or loss of protein mutations in caeruloplasmin
  • copper binding protein, loss of copper regulation massive tissue deposition of copper, especially liver and basal ganglia
  • clinical either or rarely both; neurological (chorea-athetoid movements), hepatic (cirrhosis or sub-fulminant liver failure), Kaiser Fleisher rings
  • treatment; copper chelation drugs
505
Q

Alpha 1 anti-trypsin deficiency

A
  • genetic mutations in the A1AT genes, multiple sites, causes variable phenotype
  • protein function lost excess tryptic activity
  • clinical; lung emphysema, liver deposition of mutant protein, cell damage
  • treatment; supportive management
506
Q

Describe budd-chiari

A
  • thrombosis of the hepatic veins; congenital webs, thrombotic tendency, protein c or s deficiency
  • clinical; acute-jaundice, tender hepatomegaly, chronic ascites
  • diagnosis u/s visualisation of hepatic veins
  • treatment; recanalization or TIPS
507
Q

Describe methotrexate

A
  • drugs used to treat rheumatoid arthritis and psoriasis
  • dose dependent on liver toxin; progressive fibrosis
  • clinical; no signs, monitor fibrosis
  • treatment; stop the drug
508
Q

Describe cardiac cirrhosis

A
  • secondary to high right heart pressures; incompetent tricuspid valve, congenital, rheumatic fever, constrictive pericarditis
  • clinical; CCF, with too much ascites and or liver impairment
  • treatment; treat the cardiac condition

GI (11 decks)

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