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Core Conditions > GI > Flashcards

GI Flashcards

0
Q

What is the pathogenesis of GORD ?

A
  • Weakened oesophageal sphincter, allowing stomach acid into oesophagus
  • stomach over producing acid, overflow more likely
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1
Q

How common is GORD?

A

80% of population

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2
Q

What are the lifestyle risk factors for GORD ?

A
  • obesity
  • pregnancy
  • diet: fat, choc, caffeine, alcohol, large meals
  • smoking
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3
Q

What drugs can increase risk of GORD ?

A

Anti muscarinics
Calcium channel blockers
Nitrates

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4
Q

When should GORD be investigated further/red flags

A
  • Dysphagia
  • > 55yrs
  • > 4 weeks persistent symptoms despite treatment
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5
Q

What is first line drug treatment for GORD ?

A

PPI - omeprazole 20 mg daily

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6
Q

Second line drug treatment for GORD

A

H2 receptor antagonist e.g. Ranitidine

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7
Q

First line treatment for H Pylori eradication ?

A

7 day, twice daily course:
PPI and
Amoxicillin and
Clarithromycin OR metronidazole (dependant on previous exposure)

If allergic to penicillin give
PPI, clarithromycin and metronidazole

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8
Q

Name 5 complications of GORD

A

BOROH:

  1. Barrett oesophagus
  2. Oesophageal carcinoma
  3. Reflux oesophagitis
  4. Oesophageal ulceration
  5. Hernia
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9
Q

What is the pathological change in barrett’s oesophagus ?

A

Epithelium metaplasia: squamous > columnar

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10
Q

What percentage of the population are affected by peptic ulcers ?

A

10-15%

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11
Q

Which are more common, gastric or duodenal ulcers ?

A

Duodenal (2-3x more common)

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12
Q

Where do duodenal ulcers most commonly form ?

A

Duodenal cap

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13
Q

Where do gastric ulcers most commonly form ?

A

Lesser curvature of stomach (usually in the elderly)

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14
Q

What is the pathogenesis of peptic ulcers ?

A

Breakdown of superficial epithelial cells all the way down to the muscularis mucosa (fibrous base with inflammatory cells), with no mucous protection acid breaks down stomach/duodenal wall

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15
Q

What is the most common aetiology of peptic ulcers ?

A

H pylori

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16
Q

How does h pylori cause peptic ulcers ?

A

h pylori colonises the mucosa layer of gastric Antrum via adhesion to gastric mucosal cells and causes gastritis by release of toxins:

  • CagA product is injected into epithelial cells via a pilus; changes cell morphology, replication and apoptosis
  • VacA is a pore-forming protein which increases host cell permeability, inducing apoptosis
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17
Q

What are the risk factors for peptic ulcers ?

A
  • H pylori
  • smoking (impairs mucosal healing)
  • history of reflux
  • NSAIDs
  • delayed gastric emptying/ increased gastric acid production
  • blood group O (duodenal ulcers)
  • stress (gastric ulcers)
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18
Q

Stress is a risk factor for which type of peptic ulcer ?

A

Gastric

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19
Q

Blood group O is a risk factor for which type of peptic ulcer ?

A

Duodenal

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20
Q

What is the initial treatment for peptic ulcers?

A

Offer full dose PPI or H2RA for 4-8 weeks

  • stop NSAIDS
  • H Pylori eradication
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21
Q

What are the ALARMS symptoms relating to peptic ulcers ?

A 
A- Anorexia (early satiety)
L- weight Loss
A- Anaemia
R- Recent onset of progressive symptoms
M- Melena
S- Swallowing difficulty
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22
Q

When to refer a peptic ulcer for urgent endoscopy ?

A

> 55yrs

+ ALARM symptoms (bleeding, early satiety etc)

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23
Q

Lifestyle changes for peptic ulcer disease

A

Raise head end of bed
Not eat <3hrs before going
Stop alcohol

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24
Q

A patient has burning epigastric pain that they can point to with a single finger. It is worse when they’re hungry (2-3hrs after last meal)What is the likely diagnosis of this presentation ?

A

Duodenal ulcer

  • worse 2-3hrs after food as this is when stomach contents release in to duodenum
  • gastric ulcer worse on eating*
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25
Q

Name the non-invasive tests for H Pylori

A
  • serological tests: detect IgG antibodies; 90% sensitive, 83% specific
  • 13c-urea breath test: quick, reliable, screening test; ingest 13c-urea which is broken down by urease
  • stool antigen test: immunoassay mAb for qualitative detection of H Pylori
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26
Q

What are the invasive tests for h pylori

A

Endoscopy:

  • biopsy urease test: gastric biopsies are added to a substrate containing urea and phenol red; if h pylori present, releases ammonia, causing colour to change from yellow to red
  • culture
  • histology: giemsa staining sections of gastric mucosa obtained at endoscopy
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27
Q

Rare endocrinopathy resulting in recurrent peptic ulcers ?

A

Zollinger-Ellison syndrome: gastric secreting tumours

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28
Q

What is a Cushing ulcer ?

A

Gastric ulcer caused by raised intracranial pressure stimulating vagus nerve to produce more acid (vagus nerve releases acetylcholine which stimulates m3 receptors on parietal cells and activates second messenger to stimulate hydrogen potassium pump, which will increase gastric acid production)

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29
Q

Complications if peptic ulcers

A

Haemorrhage
Perforation of ulcer
Malignancy
Gastric outflow obstruction

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30
Q

Which type of peptic ulcer is more likely to perforate ?

A

Duodenal

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31
Q

What are the 2 most common causes of acute lower GI bleed ?

A

Diverticula disease

Ischaemic colitis

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32
Q

Most common causes of upper GI bleed ?

A 
Perforated gastric ulcers
NSAIDs
Alcohol - gastric varices 
Reflux oesophagitis
Mallory-Weiss tears
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33
Q

What is the Glasgow-batchford score ?

A

Score stratifying upper GI bleeds into low and high risk based on:

  • hb level
  • BP
  • sex
  • HR
  • Melena
  • recent syncope
  • hepatic disease history
  • HF history

Zero is low risk, anything higher needs medical intervention

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34
Q

How are acute upper GI variceal bleeds treated ?

A

Terlipressin

Offer prophylactic antibiotics

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35
Q

Treatment for non variceal upper GI bleeds ?

A

Adrenaline and thermal coagulation

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36
Q

Which is more common, Crohn’s disease or ulcerative colitis ?

A

Ulcerative colitis

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37
Q

Who does Crohn’s most often affect ?

A

Females
Immunocompromised
Hispanic, Asian, Jewish

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38
Q

Deep transluminal inflammation of whole GI tract is characteristic of which condition ?

A

Crohn’s

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39
Q

Cobblestone appearance, skip lesions and granulomas are characteristic in which IBD condition ?

A

Crohn’s

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40
Q

Is Crohn’s or ulcerative colitis more likely to cause strictures and fistulas ?

A

Crohn’s

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41
Q

Superficial inflammation confined to the mucosa over the rectum, colon, appendix and terminal ileum is characteristic of which IBD condition ?

A

UC

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42
Q

Goblet cells are depleted in which IBD condition ?

A

UC

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43
Q

Which IBD condition results in the presence of inflammatory cells in the lamina propria ?

A

UC

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44
Q

What is the biggest risk factor for IBD ?

A

Familial history of IBD

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45
Q

How does s,oping affect the risk of Crohn’s and ulcerative colitis ?

A

Crohn’s - smoking increases risk

UC - smoking decreases risk

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46
Q

A presentation of history of diarrhoea with blood, RIF abdo pain and palpable mass with weight loss and anorexia is likely to be what ?

A

Chrohns disease

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47
Q

Is Crohn’s or UC more likely to have anal symptoms ?

A

Crohn’s

E.g. Oedematous anal tags, fissures, perinatal abscess

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48
Q

When is faecal calprotectin testing recommended ?

A

To support differential of IBS or IBD (+ve = IBD) when specialist investigation is being considered (if cancer not suspected)

Calprotectin is a substance that is released in excess in the intestines when inflammation is there

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49
Q

Which part of the GI tract is Crohn’s disease most likely to affect ?

A

Terminal ileum and proximal colon

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50
Q

What type of inflammation is found in Crohn’s disease ?

A

Focal, asymmetric, transmural and sometimes granulomatous inflammation

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51
Q

Which infectious agents have been linked with Crohn’s disease ?

A
  • mycobacterium paratuberculosis
  • pseudomonas spp
  • listeria spp
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52
Q

What are the theories on causes of Crohn’s ?

A
  • infectious agents
  • increase in TNF-alpha
  • high fat diet
  • genetic mutation
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53
Q

Which inflammatory bowed disease presents with skip lesions ?

A

Crohn’s

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54
Q

What ages is Crohn’s disease most likely to present ?

A

15-30 then again at 60-80

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55
Q

What age is UC most likely to present ?

A

15-25

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56
Q

What are the extraintestinal manifestations of ulcerative colitis ?

A
  • erythema nodosum
  • aphthous ulcers
  • epi scleritis
  • acute arthropathy affecting the large joints
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57
Q

What are the extraintestinal manifestations of Crohn’s disease ?

A
  • clubbing
  • erythema nodosum
  • large joint arthritis
  • fatty liver
  • osteomalacia
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58
Q

Which antibody can be tested for that is more common in Crohn’s than UC ?

A

Anti-S cerevisiae antibodies (ASCA)

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59
Q

Which antibodies can be tested for that are more common in UC than Crohn’s ?

A

Peri nuclear antineutrophil cytoplasmic antibody (p-ANCA)

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60
Q

What initial investigations should be carried out for a suspected case of IBD ?

A
  • FBC, U&Es, LFTs, ESR, CRP
  • stool culture to rule out parasites and c diff.
  • faecal calprotectin (rule out IBS)
  • serological markers (e.g. p-ANCA) or ASCA)
  • sigmoidoscopy / colonoscopy and biopsy to differentiate between macroscopic findings
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61
Q

Differential diagnoses in IBD

A
  • Crohn’s vs UC
  • Behçet’s disease
  • coeliac
  • diverticulitis
  • Ischaemic colitis
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62
Q

Which drugs can precipitate paralytic ileus and mega colon in active colitis ?

A

Antimotility drugs:
- codeine
- loperamide
Antispasmodics

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63
Q

Complications of IBD ?

A
  • toxic mega colon
  • haemorrhage
  • stricture & fistula (UC more common)
  • large bowel carcinoma
  • colorectal cancer
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64
Q

What drug is used to maintain remission in IBS ?

A

Mesalazine (aminosalicylate)

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65
Q

Which drugs induce remission in IBD ?

A

Corticosteroids

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66
Q

What percentage of the population is affected by IBS ?

A

10-20%

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67
Q

Who is IBS most likely to occur in ?

A

Women

Ages 20-30

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68
Q

What is the pathogenesis of IBS ?

A

No detectable organic cause

  • due to biopsychosocial interactions causing dysregukation of brain-gut function
  • abnormal central processing of painful stimuli
  • associated with increased psychological distress and poor coping strategies
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69
Q

What are the risk factors for IBS ?

A
  • affective disorders e.g. Anxiety, depression
  • psychological stress and trauma, life events
  • GI Infection
  • Antibiotic therapy
  • sexual, physical or verbal abuse
  • female
  • eating disorders
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70
Q

What conditions does IBS often coexist with ?

A
  • chronic fatigue syndrome
  • fibromyalgia
  • TMJ joint dysfunction
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71
Q

What are the non-GI features of IBS ?

A
  • gynae: dysmenorrhea, dyspareunia, premenstral tension
  • urinary: frequency, urgency, nocturia, incomplete emptying
  • ## other: back pain, headaches, bad breath, poor sleeping, fatigue
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72
Q

Classic presentation of IBS ?

A
  • improvement of abdo pain in defecation
  • onset of pain associated with change in frequency of stool
  • onset of pain associated with a change in appearance of stools
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73
Q

What are the non pharmacological treatments for IBS

A
  • probiotics
  • eradicate dietary triggers
  • high fibre diet and fibre supplements
  • psychotherapy, CBT
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74
Q

What investigations should be carried out to rule out other conditions if IBS suspected ?.

A
  • upper GI endoscopy (dyspepsia, reflux)
  • duodenal biopsy (coeliac)
  • giardia test
  • ## ERCP (chronic pancreatitis)
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75
Q

Pharmacological treatment for IBS ?

A
  • loperamide for diarrhoea

- mebeverine antispasmodic for colic/bloating

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76
Q

What are the risk factors for infective gastroenteritis ?

A
  • poor hygiene/lack of sanitation
  • immunocompromised
  • food hygiene/undercooked
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77
Q

By what mechanism does E. coli. Cause gastroenteritis ?

A

Mucosal adherence- adhere to receptors in the gut allowing entry of a subunit in to cell which activates adenylyl cyclase which increases amount of cAMP and results in intense and prolonged hyper secretion of chlorides and water while inhibiting reabsorption of sodium
- gut contains large amount of fluid leading to diarrhoea

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78
Q

Bloody diarrhoea in gastroenteritis would be suspicious if what causative organism ?

A

Bacterial, particularly E. coli , salmonella and shigella if from exotic location

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79
Q

What is the most common causative organism of outbreaks of gastroenteritis in the UK ?

A

Rotavirus, norovirus (winter)

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80
Q

What is the incubation period of viruses causing gastroenteritis ?

A

1 day

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81
Q

What is the incubation period for bacillary dysentery ?

A

Few hours to 4 days

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82
Q

What is the main risk to health in adult gastroenteritis ?

A

Dehydration

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83
Q

What are the signs of mild dehydration ?

A

Lassitude, anorexia, nausea, light headedness, postural hypotension

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84
Q

Features of moderate dehydration ?

A
  • Apathy
  • tiredness
  • dizziness
  • muscle cramps
  • dry tongue
  • sunken eyes
  • reduce skin elasticity
  • tachycardia
  • oliguria
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85
Q

Features of severe dehydration?

A
  • profound apathy
  • weakness
  • confusion
  • shock
  • tachycardia
  • peripheral vasoconstriction
  • BP systolic
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86
Q

When should a stool sample be sent off in an adult with gastroenteritis ?.

A
  • blood/mucous in stool *
  • immunocompromised *
  • exotic travel
  • not improved by day 7
  • uncertain diagnosis
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87
Q

What blood tests should be sent for in an unwell patient with gastroenteritis ?

A

FBC, U&Es

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88
Q

Differential diagnoses in a patient with suspected gastroenteritis

A
  • travellers diarrhoea
  • UTI
  • constipation overflow
  • IBS
  • Addison’s disease
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89
Q

Complications of gastroenteritis

A
  • haemolytic uraemic syndrome (HUS) (haemolytic anaemia, thrombocytopenia and AKI)
  • systemic invasion e.g. Salmonella
  • toxic mega colon
  • Guillain-Barré syndrome - CMV, campylobacter jejuni
  • IBS
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90
Q

What is exudative diarrhoea ?

A

Presence of pus or blood in stools

91
Q

What is the mechanism of secretory diarrhoea ?

A
  • increase in active secretion or inhibition of absorption
  • no structural damage
  • e.g. Cholera toxin: stimulates secretion of anions such as chloride, which then stimulates secretion of sodium in to lumen (to balance charge), water follows sodium –> watery diarrhoea
92
Q

Which type of diarrhoea does not stop after oral intake is stopped ?

93
Q

What is osmotic diarrhoea ?

A
  • Too much water is drawn in to lumen due to excessive molecules in lumen upsetting balance e.g. Malabsorption or excessive intake of sugar
  • stops when intake stopped
94
Q

What type of diarrhoea occurs in coeliac disease ?

95
Q

What is the pathogenesis of inflammatory diarrhoea ?

A
  • Damage to mucosal lining/brush border results in passive loss of protein rich fluid and deceased ability to reabsorb lost fluid
  • may have features of all types of diarrhoea
96
Q

Examples of causes of inflammatory diarrhoea ?

A
  • IBD

- infections

97
Q

Give an example of an opioid used as an antidiarrhoeal ?

A

Loperamide, only acts on receptors in large bowel so does not have CNS effects

98
Q

How do anticholinergics reduce diarrhoea ?

A

Reduce intestinal movements, also effective against cramp

99
Q

When do you manage gastroenteritis in hospital ?.

A

Severely dehydrated

100
Q

What antibiotic can treat gastroenteritis caused by salmonella, cholera and shigella ?

A

Ciprofloxacin

101
Q

Around what age is acute pancreatitis most likely to present ?

102
Q

How might gallstones cause acute pancreatitis ?

A
  • block bile duct causing back pressure in to main pancreatic duct
103
Q

What drugs may cause acute pancreatitis ?

A
  • thiazides
  • valproate
  • corticosteroids
104
Q

What viruses have been linked with acute pancreatitis ?.

A
  • coxsackie B
  • hepatitis
  • mumps
105
Q

Symptoms of acute pancreatitis ?

A
  • severe upper abdo pain
  • sudden onset vomiting
  • pain focused in LUQ of epigastrium and penetrates to back
  • pain decreases steadily over 72 hours
106
Q

Why might patients with acute pancreatitis present with jaundice ?

A

Gallstone in common bile duct

107
Q

What is cullen’s sign ?

A

Superficial oedema and bruising around umbilicus - can predict acute pancreatitis

(May also be seen in ruptured ectopic pregnancy, abdo trauma, aortic rupture)

108
Q

What is grey turners sign ?

A

Bruising of flanks - sign of retro peritoneal haemorrhage (pancreatic necrosis) can predict severe attack of acute pancreatitis

109
Q

What investigations should be done for acute pancreatitis ?

A
  • Bloods: serum amylase, lipase, CRP, FBC, U&Es, glucose, calcium
  • abdo x Ray: exclude perforation/obstruction and show any calcification
  • CXR: may show elevated hemi diaphragm, infiltrates and acute respiratory distress syndrome
  • ultrasound: confirm gallstones
110
Q

What would raised bilirubin and/or serum aminotransferases suggest for the cause of acute pancreatitis ?

A

Gallstones

111
Q

What are the causes of raised amylase ?

A
  • acute pancreatitis
  • renal failure
  • ectopic pregnancy
  • DKA
  • perforated duodenal ulcer
  • mesenteric infarct/Ischaemia
112
Q

What conditions cause similar pain to acute pancreatitis ?

A
  • small bowel perforation/obstruction
  • ruptured/dissecting aorta
  • atypical MI
113
Q

Which diseases are associated with acute pancreatitis ?

A
  • gallstones
  • alcoholism
  • hyperlipidaemia
  • hypothermia
114
Q

Why is morphine not used to control pain in acute pancreatitis ?

A

Linked to spasm of sphincter if Oddi (sphincter at bottom of biliary tree controlling flow of pancreatic juices and bile)

115
Q

What pain relief is used in mild cases of acute pancreatitis ?

A
  • pethidine OR buprenorphine +/- IV benzodiazepines
116
Q

When would surgery be required in acute pancreatitis ?

A

If infection and necrosis are present (debridement)

117
Q

Complications of acute pancreatitis ?

A
  • pancreatic necrosis
  • infected necrosis
  • acute fluid collections (don’t require surgery)
  • pancreatic abscess
  • acute pseudo-cyst
  • pancreatic Ascites
  • acute cholecystitis
118
Q

What shod be done for the prevention of acute pancreatitis ?

A
  • avoid alcohol
  • treat gallstones
  • plasmapheresis may reduce incidence Those with severe hypertriglyceridaemia
119
Q

Who is chronic pancreatitis most likely to affect ?

A

Males over 40, alcoholics

120
Q

Pathogenesis of chronic pancreatitis ?

A
  • obstruction or reduction of bicarbonate excretion
  • activates pancreatic enzymes
  • leads to pancreatic tissue necrosis and eventual fibrosis
  • alcohol causes proteins to precipitate in the ductal structures of the Pancreas
  • leads to local pancreatic dilatation and fibrosis
121
Q

How is large duct pancreatitis characterised ?

A
  • Dilatation and dysfunction of the large ducts - easily seen on imaging
  • diffuse pancreatic calcification
  • steatorrhoea common
  • replacement of pancreatic enzymes does not relieve pain, surgery required
122
Q

Which subtype of chronic pancreatitis occurs more in men than women ?

A

Large duct pancreatitis

123
Q

Characteristics of small duct pancreatitis ?

A
  • occurs more in women
  • not associated with calcifications
  • imaging usually normal
  • steatorrhoea rare
  • patients respond to pancreatic enzyme replacement
124
Q

Predisposing factors for chronic pancreatitis ?.

A
  • smoking
  • alcohol abuse
  • genetic - GGT1, CFTR, SPINK1 genes
125
Q

Causes of chronic pancreatitis ?

A
  • biliary tract disease
  • iatrogenic
  • metabolic disorders e.g. Hypertriglyceridaemia, hypercalcaemia
  • trauma
  • congenital e.g. CF
  • ## drugs e.g. Sulphonamides, loop diuretics
126
Q

Presentation of chronic pancreatitis ?

A
  • abdo pain: epigastric -> back
  • nausea and vomiting
  • anorexia
  • exocrine dysfunction e.g. Malabsorption and weight loss, diarrhoea, steatorrhoea, protein deficiency
  • endocrine dysfunction e.g. DM

Examination = unremarkable, tender abdo

127
Q

What bloods should be investigated Chronic pancreatitis ?

A

FBC, U&Es, LFTs, creatinine, calcium, Amylase, (usually normal), glucose, hba1c

128
Q

Complications of chronic pancreatitis ?

A
  • cobalamin deficiency
  • DM
  • percardial/pleural effusion
  • pseudo cyst
  • GI bleed (pseudo cyst invading duodenum)
  • pancreatic carcinoma
129
Q

What are the 2 most common presentations of gallstones ?

A
  • acute cholecystitis

- biliary colic

130
Q

What are the types of gallstones and what are their causes ?(4)

A
  • pigment stones: small, friable, irregular - haemolysis (radiolucent)
  • cholesterol stones: large, solitary, - age, obesity (radiolucent)
  • mixed: calcium salts, pigment, cholesterol (radiopaque)
131
Q

Risk factors for gallstones

A
  • increasing age
  • obesity
  • female
  • positive family history
  • sudden weight loss e.g. After obesity surgery
  • loss of bile salts e.g. Ileal resection
  • diabetes: as part of metabolic syndrome
  • oral contraception
132
Q

How may a gallstone cause biliary colic ?.

A

Gallstone impacts on cystic duct or ampulla of vater

133
Q

How may a gallstone cause acute cholecystitis ?

A

Distension of the gall bladder with subsequent necrosis and Ischaemia of mucosal wall

134
Q

What is the presentation of biliary colic ?

A
  • sudden epigastric/RUQ pain
  • radiates ROUND to back
  • persists for 15 mins then subsides spontaneously or with analgesia
  • nausea or vomiting often accompany pain
135
Q

Symptoms of chronic cholecystitis (caused by gall stones)

A

Vague abdominal discomfort, distension, nausea, flatulence and intolerance of fats

136
Q

Differential of gall stones ?

A
  • reflux
  • peptic ulcer
  • IBS
  • relapsing pancreatitis
137
Q

Investigations and findings for gallstones

A
  • FBC - WCC likely raised
  • liver enzymes often mildly abnormal
  • ultrasound: thickened GB wall
138
Q

Less common presentations of gallstones ?

A
  • obstructive jaundice
  • Cholangitis
  • pancreatitis
  • gallstone ileus
  • empyema
139
Q

Presentation of cholecystitis

A
  • continuous epigastric/RUQ pain
  • referred to right shoulder
  • vomiting, fever
  • local peritonism
  • GB mass
140
Q

What is the main difference between acute cholecystitis and biliary colic ?

A

Inflammatory component in cholecystitis (vomiting, fever, inc WCC)

141
Q

What may occur if a gallstone becomes lodged in the common bile duct?

A
  • obstructive jaundice

- Cholangitis

142
Q

What is murphys sign?

A
  • Place hand in RUQ just below costal margin, mid clavicular line, ask patient to breathe in.
  • pain and arrest in breathing suggests inflamed GB
  • it is only positive if same test in lower quadrant does not produce same effect*
143
Q

Symptoms of Cholangitis ?

A
  • RUQ pain
  • jaundice
  • rigors
144
Q

Treatment for Cholangitis ?

A
  • Cefuroxime and metronidazole (broad spec)

- surgical decompression of GB/endoscopic drainage

145
Q

Symptoms of obstructive jaundice ?

A
  • yellowing of skin
  • paler stools
  • darker urine
  • pruritis
146
Q

Treatment for common bile duct stones ?

A
  • Cholecystectomy and exploration of CBD if GB present
  • biliary sphincterectomy and endoscopic extraction of stone if GB previously removed
  • biliary stent if stones irretrievable
147
Q

How is hep A spread ?.

A

Faecal-oral

Shellfish

148
Q

Incubation period of hep A ?

149
Q

Symptoms of hep A ?

A
  • prodromal illnes: malaise, anorexia, nausea, arthralgia (flu like)
  • jaundice , dark urine, pale stool, itch
  • hepatomegaly, abdo pain, lymphadenopathy

*fever not actually common

150
Q

Pathophysiology of hepatitis A ?

A
  • Virus taken up by hepatocytes
  • after uptake viral RNA uncoats and host ribosome bind to form polysome
  • viral proteins then synthesised
  • assembled virus particles them shed through biliary tree into faeces
151
Q

Which parts of the world are high risk for hep A?

A
  • Indian subcontinent
  • africa
  • South and Central America
  • Middle East
152
Q

Risk factors for hep A ?

A
  • personal contact
  • occupation e.g. Sewage worker
  • travel to high risk areas
  • male homosexuality with multiple partners
  • ## IV drug use
153
Q

Conditions presenting similarly to hep a ?

A
  • other hepatitis
  • acute HIV
  • CMV
154
Q

What specific antibody tests can be done for hepatitis A ?

A
  • IgM: positive with onset of symptoms (3-6 weeks after exposure) test is sensitive and specific and remains positive for 3-6 months
  • IgG: appears soon after IgM and remains detectable for life.
155
Q

If IgG antibody for hep A is present but IgM is not, what does this suggest ?

A

Past infection or vaccination rather than active infection

156
Q

What would be found in the liver enzymes in a hep A infection?

A
  • ALT rises more than AST

- alkaline phosphate rises with ALT and AST

157
Q

Management of hep A infection?

A
  • supportive I.e. Fluid, antiemetics, rest
  • avoid alcohol until liver enzymes normal
  • admit patients with severe systemic upset or intractable vomiting for rehydration and observation
158
Q

Complications of acute hepatitis A infection ?

A
  • Cholestatic hepatitis:
  • death
  • fulminant liver disease
159
Q

Which countries is hep B most prevalent ?

A
  • subsaharan africa
  • most of Asia
  • Pacific Islands
160
Q

Most acute cases of hepatitis B in the UK are due to which cause ?

A
  • IV drug use

- sexual exposure

161
Q

Presentation of acute Hepatitis B infection ?

A
  • prodromal flu like illness
  • starts insidiously with anorexia, nausea, ache in right upper abdomen
  • icteric phase
  • *similar to hep A except arthralgia and urticaria more common
162
Q

Complications of hep b ?

A
  • liver cirrhosis
  • fulminant hepatic failure
  • cholangiocarcinoma
163
Q

Route if transmission of hepatitis b ?

A
  • vertical: mother to baby
  • sexual
  • blood to blood I.e. Sharing needles
  • transfusion associated infection (outside of UK)
164
Q

Treatment of acute hepatitis B ?

A
  • supportive
  • avoid alcohol until liver enzymes normal
  • stop any non essential meds
  • chlorphenamine for itch but avoid in sever liver impairment
  • antivirals in cases of fulminant
165
Q

What investigations should be done in suspected hep b

A
  • FBC
  • bilirubin
  • liver enzymes
  • clotting
  • ferritin
  • lipid profile
  • auto antibody screen
  • caerulopasmin
  • serological markers
  • HCV and HIV test
166
Q

Antibodies to HBsAg (I.e. Anti-HBs) imply what ?

A

Vaccination to hepatitis B only (no infection last or present)

167
Q

Antibodies to hepatitis B core antigen (HBcAg) imply what ?

A

Past infection

168
Q

Which serological marker is first to be present in hepatitis b infection ?

169
Q

Presence of HBeAg implies what ?

A

High infectivity

170
Q

What serological markers suggest chronic hep B infection .

A
  • HBsAg positive for at least 6 months

OR

  • positive HBsAg AND negative IgM HBcAg
171
Q

Route if transmission of hep C ?

A
  • mother to baby
  • sex
  • needles
172
Q

Which factors are associated with more rapid progression to severe liver disease in hep c infection ?

A
  • > 40 yrs
  • alcohol consumption
  • male gender
  • co infection with HIV HBV
173
Q

Presentation of hep c

A
  • usually asymptomatic
  • 20/30% present with jaundice or deranged liver
  • non specific - anorexia, lethargy, abdo pain
174
Q

What percentage of patients with hep c develop chronic infection ?

175
Q

Investigations in hep C ?

A
  • anti HCV serology (+ve 3-9months after exposure)
  • HCV PCR confirms ongoing infection
  • liver biopsy if HCV PCR +ve to assess liver damage
  • HCV genotype
176
Q

Complications of hep c ?

A
  • glomerulonephritis
  • cryoglobulinaemia
  • thyroiditis
  • autoimmune hep
177
Q

Which other virus does hepatitis D need in order to replicate ?.

178
Q

Affect of co infection with hep D ?

A

Acute liver failure/cirrhosis

179
Q

What are the causes of hepatitis besides hepatitis viruses?

A
  • alcohol
  • drugs
  • toxins
  • EBV/CMV
  • leptospirosis
  • malaria
  • syphilis
  • yellow fever
  • Wilson’s disease
180
Q

At what age is the highest incidence of appendicitis ?

A

10-20

However common at any age - most common surgical emergency

181
Q

Pathogenesis of appendicitis

A
  • Gut organisms invade the appendix wall after lumen obstruction by lymphoid hyperplasia, faecolith or filarial worms.
  • leads to oedema, Ischaemia, necrosis and perforation
  • cause linked to hygiene hypothesis-> impaired ability to prevent invasion
182
Q

Symptoms of appendicitis

A
  • perumbilical pain that localises to RIF
  • anorexia *
  • vomiting rarely predominant
  • constipation usual but diarrhoea may occur
183
Q

General signs seen in a patient with appendicitis ?

A
  • tachycardia
  • fever
  • furred tongue, foetor oris
  • lying still
  • shallow breaths
    In the RIF: guarding, rebound and percussion tenderness
184
Q

What is McBurney’s sign ?

A

Sign of acute appendicitis:

  • pain at point 1/3 of way from ASIS to umbilicus
  • suggests inflammation no longer limited to lumen of bowel (which localises pain poorly) is now irritating lining if peritoneum
  • suggests increased likelihood of rupture
185
Q

Investigations and findings in acute appendicitis

A
  • bloods: CRP elevated, neutrophil leucocytosos
  • ultrasound may help but appendix not always visualised
  • CT has high diagnostic accuracy if unclear however may cause fatal delay
186
Q

Treatment for appendicitis

A
  • prompt appendectomy (if unsure examine often to avoid removing normal appendix)
  • abx: metronidazole and cefuroxime
187
Q

Complications of appendicitis

A
  • perforation

- appendix abscess

188
Q

Pain from the fore gut radiates where ?

Prox to 2nd part of duodenum

A

Epigastrium

189
Q

Where does pain from mid gut radiate to ?

Above to 2/3 along transverse colon

A

Perumbilical

190
Q

Where does the hind gut radiate to ?

A

Supra public

191
Q

Which conditions present similarly to appendicitis ?

A
  • ectopic pregnancy
  • UTI
  • mesenteric adenitis
  • Crohn’s disease
  • diverticulitis
  • perforated ulcer
192
Q

Cardinal features of intestinal obstruction ?

A
  • vomiting
  • colicky pain
  • constipation
  • distension
193
Q

Causes of small bowl obstruction

A
  • adhesions

- hernias

194
Q

Causes of large bowel obstruction ?

A
  • constipation
  • colorectal carcinoma
  • diverticular stricture
  • volvulus - sigmoid or caecal
195
Q

Features if a small bowl obstruction

A
  • vomiting occurs earlier
  • distension is less
  • pain higher in abdomen
196
Q

Findings on AXR of small bowel obstruction a

A
  • central gas shadows
  • valvulae conniventes that completely cross lumen
  • no gas in large bowel
197
Q

Features specific to large bowel obstruction ?

A
  • vomiting later
  • absolute constipation more likely
  • more distension
  • pain more constant
198
Q

Findings on AXR of large bowel obstruction

A
  • peripheral gas shadows proximal to blockage

- large bowel haustra do not cross all lumens width

199
Q

What is an ileus and what are its clinical features ?

A
  • a functional obstruction from reduced bowel motility
  • no pain
  • bowel sounds absent
200
Q

What is a simple obstruction ?

A
  • One obstruction point

- no vascular compromise

201
Q

What is a closed loop obstruction ?

A
  • obstruction at 2 points
  • forming a loop of grossly distended bowel
  • risk if perforation
202
Q

Which point in the bowel is most likely to perforate and why
.

A

Caecum - where bowel is thinnest and widest

203
Q

What is a strangulated bowl obstruction ? What are its features?

A
  • blood supply is compromised
  • patient more ill than would expect
  • sharper, more constant and localised pain
  • peritonism = Cardinal sign
  • fever with increased WCC and other signs of mesenteric Ischaemia
204
Q

Which types of bowel obstruction always need surgery ?

A
  • strangulation obstructions - emergency
  • closed loop obstructions - emergency
  • large bowel obstructions
205
Q

What are the immediate actions once bowel obstruction is diagnosed ?

A
  • NGT and IV fluids
  • analgesia
  • bloods: amylase, FBC, U&Es
  • AXR
  • erect CXR
  • catheterise and monitor fluid status
206
Q

What is meant by an irreducible hernia ?

A
  • cannot be pushed back into the right place

- refers to bowel hernias

207
Q

What is meant by an incarceration hernia ?

A

Implies the contents of hernial sack are stuck inside by adhesions

208
Q

When are GI hernias considered obstructed ?

A

If bowel contents cannot pass through them

209
Q

When is a hernia considered strangulated ?

A

If Ischaemia occurs

210
Q

Who do femoral hernias more commonly present in ?

A

Women, middle aged and elderly

211
Q

Where are femoral hernias felt in relation to the pubic tubercle ?

A

Inferior and lateral

212
Q

Where are inguinal hernias felt in relation to the pubic tubercle ?

A

Superior and medial

213
Q

Pathogenesis of femoral hernia

A
  • Bowel enters the femoral canal
  • presents mass in upper medial thigh or above inguinal ligament
  • mass points down the leg
214
Q

Conditions presenting similarly to femoral hernia ?

A
  • inguinal hernia
  • enlarged cloquets node
  • lipoma
  • femoral aneurysm
215
Q

Treatment for femoral hernia ?

A

Surgical repair (herniotomy- ligation and excision if of the sac & herniorrhaphy - repair of hernial defect)

216
Q

What are direct inguinal hernias ?

A

Hernia push their way directly forward through the posterior wall of the inguinal canal, into a defect in the abdominal wall

217
Q

Risk factors for direct inguinal hernia ?.

A
  • male
  • chronic cough
  • constipation
  • urinary obstruction
  • heavy lifting
  • Ascites
218
Q

What are the borders of the inguinal canal:

A
  • floor: inguinal ligament
  • roof: fibres of transversalis, internal oblique
  • anterior: external oblique aponeurosis & internal oblique for lat 1/4
  • post: laterally= transversalis fascia, med= conjoint tendon
219
Q

Which type of inguinal hernia is more likely to strangulate ?

220
Q

What are indirect inguinal hernias ?

A

Hernia through patent processus vaginalis

221
Q

What does tissue transglutaminase antibody test for ?

A

Coeliac disease

222
Q

Which is more painful and why- intra abdominal bleed or bile leak ?

A

Bile leak as bile more irritant than blood

223
Q

What day post op does wound dehiscence usually occur ?

224
Q

What is the most common post operative complication in older men ?

A

Acute urinary retention

225
Q

Vague abdo symptoms e.g. Bloating and intermittent discomfort with steatorrhoea and weight loss is suspicious of which diagnosis ?

Core Conditions (15 decks)

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