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Phase 2 > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

Define intestinal obstruction

A

Blockage to the lumen of the gut - often refers to blockage of the intra-abdominal part of the intestine

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2
Q

How do we classify bowel obstructions

A
  1. According to site
    - Large/Small bowel/Gastric
  2. Extent of luminal obstruction
    - Partial/complete
  3. According to mechanism
    - Mechanical
    - Paralytic
  4. According to pathology
    - Simple
    - Closed loop
    - Strangulation
    - Intussusception
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3
Q

What percentage of intestinal obstruction occurs in the small bowel

A

60-75%

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4
Q

Describe the pathophysiology of small bowel disease

A

Bowel obstruction leads to bowel distension with increased secretion of fluid into the distended bowel leading to proximal dilation above the block

Increased secretion, swallowed air and bacterial fermentation lead to more dilation

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5
Q

What are the three results of untreated obstruction in the small bowel

A

Ischaemia
Necrosis
Perforation

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6
Q

What percentage of bowel obstructions is due to large bowel obstruction

A

25%

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7
Q

What is the pathophysiology of large bowel obstruction

A

Colon proximal to obstruction dilates and increased colonic pressure leads to decreased mesenteric blood flow resulting in mucosal oedema

This causes the arterial blood supply to become compromised leading to necrosis and perforation

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8
Q

What happens if the ileocaecal valve is competent in bowel obstruction

A

Caecum dilates and patient won’t feel unwell but will have massive distension

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9
Q

What happens if the ileocaecal valve is incompetent in bowel obstruction

A

Faeculent vomiting

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10
Q

What are the three different types of bowel obstruction

A

Intaluminal - something in the bowel

Intramural = something in the wall of the bowel

Extraluminal = something outside the bowel

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11
Q

What are the causes of intraluminal obstruction

A

Tumour
- Carcinoma and lymphoma

Diaphragm disease
- Fibrous fold in lumen

Meconium Ileus
- Content of neonate bowel becomes sticky

Gallstone Ileus
- Stone gets stuck in small bowel by eroding through gall bladder

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12
Q

Diaphragm disease is associated with what

A

NSAIDs

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13
Q

What are the causes of intramural obstruction

A
  1. Inflammatory disease
    - Crohn’s/diverticulitis/ulcerative colitis
  2. Tumours in bowel wall
  3. Hirschsprung’s disease
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14
Q

What is Crohn’s disease

A

Fibrosis of the bowel wall producing a cobblestone mucosa and granulomas

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15
Q

What is the pathophysiology of diverticular disease

A

Inflammation an fibrosis in the sigmoid colon - In low fibre diet mucosa is pushed through gaps in the muscular wall of the bowel due to increased pressure resulting in diverticulae

These act as cul de sacs where faeces can remain and become inflamed and rupture causing faecal peritonitis

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16
Q

What is Hirschsprung’s disease

A

Aganglionic segment of the bowel where there is no nerves meaning the bowel doesn’t contract leading to distal distension

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17
Q

What are the causes of extraluminal obstruction

A

Adhesions
Volvus
Intussusception
Peritoneal tumour

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18
Q

What is an adhesion

A

Fibrous band that sticks two bits of bowel together and the bowel is pulled and distorted
Normally seen post abdominal surgery

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19
Q

What is Volvulus

A

Bowel twisting around each other which cuts off blood supply = closed loop obstruction

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20
Q

What is intussusception

A

One part of intestine telescopes inside another

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21
Q

Where does a peritoneal tumour normally originate from

A

Ovarian cancer which spreads onto the peritoneum

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22
Q

What ares of the bowel of most likely to be affected with Volvos

A

Areas of the bowel with a mesentery ie. sigmoid colon

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23
Q

What are the causes of small bowel obstruction in adults

A
  1. Adhesions
  2. Hernia
  3. Crohns
  4. Malignancy
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24
Q

What are the causes of small bowel obstruction in children

A 
Appendicitis 
Intesussception 
Volvus 
Atresia 
Hypertrophic pyloric stenosis
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25
Q

What are the two types of intesussuption

A

Idiopathic

Enteroenteral Intersussception

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26
Q

What is enteroenteral intersussception associated with

A

Cystic fibrosis

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27
Q

What are the uncommon causes of a small bowel obstruction

A 
Radiation 
Gallstones 
Diverticulitis and Appendicitis 
Sealed small perforation 
Foreign bodies (Bezoars)
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28
Q

What are the symptoms of small bowel obstruction

A
  1. Early feculent projectile vomit
  2. Diffuse colicky pain
  3. Late constipation
  4. Distension
  5. Tenderness
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29
Q

What investigations might you do in someone who you suspect to have a small bowel obstruction?

A

Take a good history - ask about previous surgery (adhesions)!

  1. FBC, U+E, lactate.
  2. X-ray.
  3. CT, ultrasound, MRI.
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30
Q

What is the management/treatment for small bowel obstruction?

A
  1. Fluid resuscitation.
  2. Bowel decompression.
  3. Analgesia and anti-emetics.
  4. Antibiotics.
  5. Surgery e.g. laparotomy, bypass segment, resection
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31
Q

What are the causes of large bowel obstruction

A
  1. Age and race dependent
    - Colorectal malignancy
    - Volvulus
    - Ischaemic structures
    - hernia
  2. Paediatric
    - Imperforate anus
    - Hirschsprung disease
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32
Q

What are the symptoms of large bowel obstruction

A 
Abdominal discomfort 
Fullness 
Bloating 
Distension 
Late vomiting 
Colicky pain 
Obstipation 
Volvulus 
Sudden pain 
Localised tenderness
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33
Q

What investigations might you do in someone who you suspect to have a large bowel obstruction?

A
  1. Digital rectal examination.
  2. Sigmoidoscopy.
  3. Plain X-ray.
  4. CT scan.
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34
Q

Describe the management for a large bowel obstruction.

A
  1. Fast the patient.
  2. Supplement O2.
  3. IV fluids to replace losses and correct electrolyte imbalance.
  4. Urinary catheterisation to monitor urine output.
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35
Q

Describe the progression from normal epithelium to colorectal cancer.

A
  1. Normal epithelium.
  2. Adenoma.
  3. Colorectal adenocarcinoma.
  4. Metastatic colorectal adenocarcinoma.
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36
Q

Define adenocarcinoma

A

A malignant tumour of glandular epithelium.

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37
Q

What is familial adenomatous polyposis?

A

Familial adenomatous polyposis is a genetic condition where you develop thousands of polyps in your teens.

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38
Q

Describe the pathophysiology of familial adenomatous polyposis.

A

There is a mutation in apc protein and so the apc/GSK complex isn’t formed -> beta catenin cannot be broken down so levels increase -> up-regulation of adenomatous epithelium gene transcription –> Adenoma forms

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39
Q

Describe the pathophysiology of Hereditary Non-Polyposis Colorectal Cancer.

A

There are no DNA repair proteins meaning there is a risk of colon cancer and endometrial cancers.

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40
Q

What are the implications of hereditary non-polyposis colorectal cancer

A

Cant use DNA damaging chemo as lack of DNA repair gene means DNA damage cant be recognised so apoptosis not activated

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41
Q

Where is the most common location for colorectal cancer

A

Sigmoid colon/rectum

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42
Q

How can adenoma formation be prevented?

A

NSAIDS are believed to prevent adenoma formation

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43
Q

What is the treatment for adenoma?

A

Endoscopic resection.

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44
Q

What is the treatment for colorectal adenocarcinoma?

A

Surgical resection can be done when there is no spread. Remember to balance risks v benefits. The patient has a pre-op assessment.

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45
Q

What is the treatment for metastatic colorectal adenocarcinoma?

A

Chemotherapy and palliative care

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46
Q

Give 3 reasons why bowel cancer survival has increased over recent years.

A
  1. Introduction of the bowel cancer screening programme.
  2. Colonoscopic techniques.
  3. Improvements in treatment options.
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47
Q

Give 5 risk factors for colorectal cancer.

A
  1. Low fibre diet.
  2. Diet high in red meat.
  3. Alcohol.
  4. Smoking.
  5. A PMH of adenoma or ulcerative colitis.
  6. A family history of colorectal cancer; FAP or HNPCC
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48
Q

What are the symptoms of a left sided sigmoid cancer

A

rectal bleeding, altered bowel habit/obstruction, colicky pain

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49
Q

What are the symptoms of a right sided sigmoid cancer

A

iron deficiency anaemia, R iliac fossa mass, weight loss

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50
Q

What investigations might you do in someone who you suspect might have colorectal cancer?

A

Colonoscopy = gold standard!
It permits biopsy and removal of small polyps.
- Tumour markers are good for monitoring progress.
- Faecal occult blood is used in screening but not diagnosis.

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51
Q

Describe the coding system for resection of tumours

A 
R0 = tumour completely excised locally 
R1 = Microscopic involvement of margin by tumour 
R2 = Macroscopic involvement of margin by tumour
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52
Q

Describe the staging system for cancer

A
  • T – T1 (invades submucosa) -> T2 (muscularis propria) -> T3 (bowel wall) -> T4 (peritoneum)
  • N – N1 (spread to lymph nodes) -> N2 (spread to lymph nodes above diaphragm)
  • M – M1 = surrounding structure involvement (liver)
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53
Q

What are the non-infectious causes of diarrhoea

A 
hormonal 
Radiation 
Chemical 
Anatomical 
Irritable bowel 
Inflammatory 
Neoplasm
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54
Q

Name some causative agents of diarrhoea

A 
Rotavirus 
Shigella 
E.coli 
Salmonella type 
Salmonella paratyphoid 
Hepatitis A 
Hepatitis E 
Vibrio cholerae
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55
Q

Define gastroenteritis

A

Diarrhoea +/- vomiting due to an enteric infection

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56
Q

Define acute diarrhoea

A

3+ episodes of partially formed watery stools for <14 days

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57
Q

Define dysentery

A

Infectious diarrhoea and blood

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58
Q

Define travellers diarrhoea

A

Gastroenteritis occurring under 2 weeks after entering a new country

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59
Q

What is the pathogenesis of norovirus

A

Single strand RNA

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60
Q

What are the symptoms of norovirus

A

Vomiting
Watery diarrhoea
Cramps
Nausea

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61
Q

What is the treatment for norovirus

A

Self limiting disease

Supportive with loperamide

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62
Q

What Id the pathophysiology of rotavirus

A

Double stranded DNA

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63
Q

What are the symptoms of rotavirus

A

2-day incubation –> 3-8 day symptoms

Watery diarrhoea
Vomiting
fever
Abdominal pain

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64
Q

What is the management of rotavirus

A

Prevention through vaccination

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65
Q

ETEC is the most common cause of what

A

Traveller’s Diarrhoea

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66
Q

What is the pathophysiology of ETEC

A

Gram -ve bacillus anaerobe that is heat stable toxin

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67
Q

What are the symptoms of ETEC

A

1-3 day incubation with 3-4 days symptoms

Watery diarrhoea and cramps

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68
Q

What is the management of ETEC

A

Rehydration

Anti-motility agents (Loperamide)

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69
Q

What is the pathophysiology of clostridium perfringens

A

Gram +ve anaerobe which produces enterotoxins

Spores survive cooking and multiply in unrefrigerated storage

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70
Q

What are the symptoms of clostridium perfringens

A

sudden onset diarrhoea and cramps normally for 24hr

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71
Q

What is the management of clostridium perfringens

A

Supportive

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72
Q

What is the pathophysiology of vibrio cholerae

A

Gram -ve flagellated aerobe vibrio transmitted by faecally contaminated water

Servers 01 and 0139 are pathogenic

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73
Q

What are the symptoms of vibrio cholerae

A 
2-5 days incubation 
Rice water stools 
Vomiting 
Dehydration
Circulatory collapse = death
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74
Q

What is the management of vibrio cholerae

A

Prevention through clean water and vaccination

Treatment with oral rehydration salts/IV rehydration and antibiotics

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75
Q

What is the pathophysiology of shigella

A

Gram -ve

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76
Q

What are the symptoms of shigella

A 
1-2 days incubation and 5-7 day symptoms 
Watery/bloody diarrhoea
Pain 
Cramping rectal pain 
Fever
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77
Q

What is the management of shigella

A

Supportive
Zinc for children
Antibiotics (Ciprofloxacin and azithromycin)

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78
Q

What is the pathophysiology of campylobacter jejuni

A

Gram -ve bacillus - very common in meat and milk

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79
Q

What are the symptoms of campylobacter jejuni

A 
2-5 day incubation 
Bloody diarrhoea
Pain 
Fever 
Headache
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80
Q

What is the management of campylobacter jejuni

A

Supportive - antibiotics if invasive (Macrolide and doxycycline)

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81
Q

What is the pathophysiology of salmonella enterocolitis

A

gram -ve anaerobic bacilli

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82
Q

What are the symptoms of salmonella enterocolitis

A 
12-36hr exposure 
Bloody diarrhoea 
Crampls 
Fever 
Invasive infection = sepsis, meningitis, osteomyelitis
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83
Q

What is the management of salmonella enterocolitis

A

Supportive - antibiotics for invasive infection (Quinolone and macrolide)

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84
Q

What is the pathophysiology of clostridium difficile

A

Gram +ve aerobic bacilli that produces enterotoxin A and B

Antibiotic use destroys the competing flora so there is less inhibition of C.diff

Spread by the faeco-oral route

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85
Q

Symptoms of clostridium difficile

A

Watery diarrhoea

Fulminant colitis

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86
Q

How would you investigate someone thought to have C.diff

A

Test stool samples for toxins

Tissue samples obtained at sigmoidoscopy

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87
Q

What antibiotics can cause C.diff

A

Clindamycin
Ciprofloxacin
Co-amoxiclav
Cephalosporins

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88
Q

What is the treatment for C.diff

A

Metronidazole

Vancomycin

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89
Q

Name some other causes of gastroenteritis

A

Protozoa (Giardia, cryptosporidium)

Helminths (Schistosome, strongyloide)

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90
Q

How can we prevent diarrhoea

A
  1. Rotavirus and measles vaccination
  2. Promote early breastfeeding
  3. Promote hand washing with soap
  4. Improve water supply quantity and quality
  5. Community wide sanitation promotion
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91
Q

What groups are most at risk of diarrhoea

A
  1. Persons of doubtful hygiene or unsatisfactory hygiene at home, work or school
  2. Children who attend pre-school or nursery
  3. People who work in preparing or serving unwrapped/uncooked food
  4. Health care workers or social care staff working with vulnerable people
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92
Q

What is a notifiable disease

A

Diseases, infections and conditions specifically listed as notifiable under public health

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93
Q

Name some examples of notifiable diseases

A 
Anthrax
Cholera 
Plague 
Rabies 
SARS
Smallpox 
Yellow fever 
Leprosy 
Malaria 
Botulism
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94
Q

Name some examples of vaccine preventable diseases

A 
Diptheria 
Measles 
Mumps 
Rubella 
Tetanus 
Whooping cough 
Acute meningitis 
Meningococcal septicaemia
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95
Q

What diseases need specific control measures

A 
Acute infectious hepatitis 
Foodborne 
 - food poisoning 
 - botulism 
 - Enteric fever 
 - infectious blood diarrhoea 
Scarlet fever 
Tuberculosis
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96
Q

What are some diseases notifiable

A

Very dangerous
Vaccine preventable
Diseases that need specific control measures

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97
Q

What is the role of surveillance in notifiable diseases

A

Detection of any changes in disease

  • Outbreak detection
  • Early warning
  • Forecasting

Track changes in disease

  • Extent and severity of disease
  • Risk factors
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98
Q

How do you protect a community from notifiable disease

A

Investigate - control tracing, partner notification, lookback exercises

Identify and protect vulnerable people
(Chemoprophylaxis, immunisation and isolation)

Exclude high risk persons from high risk settings

Educate, inform, raise awarnesss and promote health

Coordinate multi-agency responses

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99
Q

What are the steps that must be taken when notifying about a disease

A
  1. Notification
    - all suspected cases without delay
  2. Contact tracing
    - Any person with close contact in past 7 days
  3. Prophylaxis
    - Advice (warn about symptoms and glass spot tests)
    - Antibiotics chemoprophylaxis (Close contacts, ciprofloxacin and rifampicin)
    - Immunisation (If available serogroup)
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100
Q

What are the two forms of active immunity

A

Cell mediated immunity

Antibody mediated immunity

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101
Q

What is passive immunity

A

Protection provided from the transfer of antibodies from immune individuals

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102
Q

What is the most common form of passive immunity

A

Cross placental transfer of antibodies from mother to child or via transfusion of blood or blood products

Protection is temporary

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103
Q

Describe passive immunisation through the use of human normal immunoglobulin

A

Increases the persons antibody level to that specific infection providing protection
From plasma donors and contains antibodies to infectious disease currently prevalent

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104
Q

When is human normal immunoglobulin used

A 
Immunocompromised children 
Tetanus 
Hepatitis B 
Rabies 
Varicella Zoster
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105
Q

What is an active immunisation

A

Vaccination stimulates immune response and memory to a specific antigen/infection

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106
Q

What are vaccines made from

A

inactivated (Killed) (Pertussis, inactivated polio)

Attenuated live organisms (yellow fever, MMR, polio and BCG)

Secreted products (Tetanus, diphtheria toxoids)

Constituents of cell walls (HepB) or recombinant components (Experimental)

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107
Q

Define vaccine failure

A

Small proportion of individuals get infected despite vaccination

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108
Q

Define primary vaccine failure

A

Persons doesn’t develop immunity from vaccine

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109
Q

Define secondary vaccine failure

A

Initially responds but protection wanes overtimes

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110
Q

What are the two presentations of meningococcal infection

A

Meningitis

Septicaemia

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111
Q

Meningococcal infection is caused by what

A

Neisseria meningitidis

Serogroups B, C, A, Y and W135

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112
Q

How is meningococcal infection spread

A

Person to person by inhaling respiratory secretions from mouth and throat or by direct contact (kissing)

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113
Q

What can meningococcal infection cause

A 
Brain abscess 
Brain damage 
Seizure disorder 
Hearing impairment 
Focal neurological disorders 
Organ failure
 Gangrene
Auto-amputation 
Death
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114
Q

What is the management of meningococcal infection

A

Antibiotic therapy: Cefotaxime and ceftriaxone

Supportive therapy

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115
Q

What are the routine childhood immunisations

A

Meningitis C vaccine
meningitis B vaccine
Quadrivalent (A, C, W135, Y)

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116
Q

What immunisations are given the eight week baby check

A

Diptheria, tetanus, pertussis, polio, heaemophilus influenza type B

Pneumococcal

Meningococcal group B

Rotavirus gastroenteritis

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117
Q

What can helicobacter pylori infection cause?

A

H.pylori produces urease -> ammonia -> damage to gastric mucosa -> neutrophil recruitment and inflammation. This can cause gastritis; peptic ulcer disease and gastric cancer.

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118
Q

Describe h.pylori.

A

A gram negative bacilli with a flagellum.

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119
Q

Describe the treatment for H.pylori infection.

A

Triple therapy: 2 antibiotics and 1 PPI e.g. omeprazole, clarithromyocin and amoxicillin.

120
Q

Define hernia

A

Abnormal protrusion of an organ into a body cavity

121
Q

Give 2 symptoms of a hernia

A

Pain

Palpable lump

122
Q

Define irritable bowel syndrome

A

Disorders of enhanced visceral perception - bowel symptoms for which no organic cause can be found

123
Q

What are the causes of IBS

A 
Unknown 
Stress
Food 
Gastroenteritis or menstruation 
Depression/Anxiety 
Psychosocial stress and trauma 
GI infection 
Sexual, physical or verbal abuse
124
Q

Describe the multi-factorial pathophysiology of IBS.

A

The following factors can all contribute to IBS:

  • Psychological morbidity e.g. trauma in early life.
  • Abnormal gut motility.
  • Genetics.
  • Altered gut signalling (visceral hypersensitivity).
125
Q

Describe the epidemology of IBS

A

More common in women

Age of onset <40

126
Q

When should you consider IBS as a diagnosis (Think ABC)

A

If patients reports

  1. Abdominal pain or discomfort
  2. Bloating
  3. Change in bowel habit
127
Q

Give 3 symptoms of IBS.

A
  1. ABDOMINAL PAIN!
  2. Pain is relieved on defecation.
  3. Bloating.
  4. Change in bowel habit.
  5. Mucus.
  6. Fatigue.
128
Q

What is the diagnostic criteria for IBS

A

ROME criteria
Abdominal discomfort/pain for > 12 weeks which has 2 of the following
- Relieved by defecation
- Change in stool frequency
- Change in stool form (Pellets, mucus)

+ 2 of

  • Urgency
  • Incomplete evacuation
  • Abdominal bloating/distension
  • Mucous pro rectum
  • Worsening symptoms after food
129
Q

What are the exclusion criteria for IBS

A 
>40yrs 
Bloody stool 
Anorexia 
Wt loss 
Diarrhoea at night
130
Q

Give an example of a differential diagnosis for IBS.

A
  1. Coeliac disease.
  2. Lactose intolerance.
  3. Bile acid malabsorption.
  4. IBD.
  5. Colorectal cancer.
131
Q

What investigations might you do in someone with IBS

A
  1. Bloods - FBC, U+E and LFT
  2. Coeliac serology
  3. CRP
  4. Colonoscopy if >60 years
132
Q

What are the treatments for mild IBS

A 
Education 
Reassurance 
Dietary modification 
 - Decreased processed food 
 - Low FODMAP diet 
 - Regular small meals 
 - Plenty of fluids 
 - Avoid caffeine, alcohol + fizzy drinks
133
Q

What are the pharmacotherapy options for IBS

A

Laxatives (Mavicol) for constipation

Loperamide (Anti-motility) for diarrhoea

Antispasmodics (Mebeverine/buscopan) for colic/bloating

CBT and amitriptyline

134
Q

What are the treatment options for severe IBS

A

MDT approach and amitriptyline

135
Q

What are the non-intestinal symptoms of IBS

A

Painful period
Urinary frequency
Back pain
Fatigue

136
Q

Define dyspepsia

A

An inexact term used to describe a number of abdominal symptoms

137
Q

What is the criteria for dyspepsia

A

> 1 of the following

  • Post prandial fullness
  • Early satiation
  • Epigastric pain/burning
138
Q

What are the symptoms of dyspepsia

A 
Epigastric pain 
Bloating 
Heartburn 
Acidity 
Nocturnal cough
Hoarse voice 
Fullness
139
Q

Give 5 causes of dyspepsia

A 
GORD
Gastritis 
Peptic ulcer disease 
Excess acid 
Prolonged NSAIDs 
Large volume meals 
Obesity 
Smoking/alcohol 
Pregnancy
Oesophageal or stomach cancer 
non ulcer dyspepsia
140
Q

Give 5 red flag symptoms that you might detect when taking a history from someone with dyspepsia.

A 
Anaemia 
Loss of wt 
Anorexia 
Recent onset progressive symptoms 
Melaena or haematemesis 
Swallowing difficulty
141
Q

What investigations might you do in someone with dyspepsia

A

Endoscopy
Gastroscopy
Barium swallow
Capsule endoscopy

142
Q

What is the management for dyspepsia if the red flag criteria has been met?

A
  1. Suspend NSAID use and review medication.
  2. Endoscopy.
  3. Refer malignancy to specialist.
143
Q

What is the management for dyspepsia without red flag symptoms?

A
  1. Review medication.
  2. Lifestyle advice.
  3. Full dose PPI for 1 month.
  4. Test and treat h.pylori infection.
144
Q

What kind of lifestyle advice might you give to someone with dyspepsia?

A
  1. Lose weight.
  2. Stop smoking.
  3. Cut down alcohol.
  4. Dietary modification.
  5. Stop NSAIDs
  6. Avoid hot drinks
145
Q

Define GORD

A

Exists when reflux of stomach contents causes troublesome symptoms - 2 or more heartburn episodes a week with or without complications

146
Q

What is the pathophysiology of GORD

A

Lower oesophageal sphincter dysfunction leads to reflux of gastric contents and oesophagitis –> Prolonged exposure leads to Barret’s oesophagus

147
Q

What are the causes of GORD

A
  1. Reduced lower oesophageal sphincter tone
  2. Hiatus hernia
  3. increased mucosal sensitivity to gastric acid and reduced oesophageal acid clearance
  4. Gastric acid hypersecretion
  5. Alcohol
  6. Delayed gastric emptying an prolonged post prandial
148
Q

What are the risk factors of GORD

A 
Hiatus hernia 
Smoking 
EtOH
Obesity 
Pregnancy 
Drugs 
Large meals
149
Q

What are the oesophageal symptoms of GORD

A

Heartburn

  • Related to meals
  • Worse lying down/stooping
  • Relieved by antacids
  • Worse with hot drinks and alcohol
Belching 
Acid regurgitation (Acid brash)
Increased salivation (Water brash)
Odonophagia (Pain swallowing)
150
Q

What are the extra-oesophageal symptoms of GORD

A

Nocturnal asthma
Chronic cough
Laryngitis
Sinusitis

151
Q

What are the complications of GORD

A 
Oesophagitis = heartburn 
Ulceration - haematemesis 
Benign stricture = dysphagia 
Barrett's oesophagus 
Oesophageal adenocarcinoma
152
Q

What Is the pathophysiology of Barrett’s oesophagus

A

Intestinal metaplasia of squamous epithelium to columnar epithelium leading to dysplasia and adenocarcinoma

153
Q

What is the differential diagnosis of GORD

A 
Oesophagitis 
PUD
Oesophageal cancer 
NSAIDs
Herpes
154
Q

What are the investigations for someone with GORD

A

Endoscopy if

  • > 55yrs
  • symptoms >4 weeks
  • Dysphagia
  • Wt loss

Bloods - FBC

CXR - may show hiatus hernia

Barium swallow

155
Q

What are the conservative measures for treatment of GORD

A 
Lose Wt 
Small regular meals 
Avoid eating within 3 hours of bed 
Stop smoking 
Decrease alcohol 
Avoid hot drinks and spicy food 
Stop drug (NSAIDs, Steroids
156
Q

What is the medical management of GORD

A

Antacids (gaviscon)
1. Full dose proton pump inhibitor (Lansoprazole)

  1. No response then double lansoprazole dose
  2. No response then add a H2 receptor antagonist such as Ranitidine
  3. Surgery - Nissen Fundoplication
157
Q

When is the Nissen fundoplication procedure indicated in the treatment of GORD

A

All three of
Severe symptoms
Refractory t medical therapy
Confirmed reflux

158
Q

What is the aim of the Nissen fundoplication procedure

A

Aims to laparoscopically increase resting lower oesophageal sphincter pressure to prevent reflux

159
Q

What are the 2 types of hiatus hernia

A

Sliding (80%)

Rolling (15%)

160
Q

What is a sliding hiatus hernia

A

When the gastro-oesophageal junction slides up into the chest to lie above the diaphragm

161
Q

What is a rolling hiatus hernia

A

Gastro-oesophageal junction remains in abdomen but a bulge of stomach rolls into chest alongside the oesophagus

162
Q

What investigations would you carry out in someone with suspected hiatus hernia

A

CXR - gas bubble and fluid level in chest

Ba swallow

OGD

163
Q

What is the treatment for hiatus hernia

A

Lose Wt
Treat the reflux
Surgery

164
Q

Smoking is protective in ulcerative colitis or Crohns

A

Ulcerative colitis

165
Q

Smoking is damaging in ulcerative colitis or Crohns

A

Crohns

166
Q

What age does ulcerative colitis present

A

30’s

167
Q

What age does crohn’s disease present

A

20’s

168
Q

Where is ulcerative colitis found

A

In the rectum up to the colon but no further

169
Q

Where is crohn’s disease found

A

From the mouth to the anus and especially in the terminal ileum

170
Q

Describe the distribution of ulcerative colitis

A

Continguous

171
Q

Describe the distribution of crohns

A

Skip lesions

172
Q

Do you get strictures in ulcerative colitis

A

No

173
Q

Do you get skip lesions in crohn;s disease

A

Yes

174
Q

Where dies the inflammation occur in ulcerative colitis

A

Mucosal - mainly in crypts leading to abscesses

175
Q

Where does the inflammation occur in crohn’s

A

Transmural

176
Q

Describe the ulcers found in ulcerative colitis

A

Shallow and broad

177
Q

Describe the ulcers found in Crohn’s disease

A

Deep, thin producing a cobblestone mucosa

178
Q

Are there granulomas in ulcerative colitis

A

No

179
Q

Are there granulomas in crohns

A

yes

180
Q

Do you get fistulas in ulcerative colitis

A

No

181
Q

Do you gt fistulas in crohns

A

Yes

182
Q

What are the systemic symptoms of ulcerative colitis and crohns

A

Fever
Malaise
Anorexia
Weight loss

183
Q

What are the abdominal symptoms in ulcerative colitis

A

diarrhoea
Blood and mucus
Abdominal discomfort
Faecal urgency

184
Q

What are the abdominal symptoms in Crohn’s

A

Diarrhoea (Not bloody)
abdominal pain
Weight losss
Failure to thrive

185
Q

What are the extra-abdominal symptoms of ulcerative colitis and Crohns

A

Skin

  • Clubbing
  • erythema nodosum
  • Pyoderma gangrene

Eyes

  • Iritis
  • Conjunctivitis
  • Uveitis

Joints

  • Arthritis
  • Ankylosing Spondylitis

HPB

  • PSC nd cholangiocarcinoma
  • Gallstones
  • Fatty liver

Other
- Amyloidosis

186
Q

What are the complications of ulcerative colitis

A

Toxic megacolon leading to blood loss, colorectal cancer, cholangiocarcinoma and toxic dilatation

187
Q

What are the complications of crohns disease

A 
Fistulae 
Strictures leading to obstruction 
Abscesses 
Malabsorption
Toxic Megacolon
188
Q

What are the risk factors for ulcerative colitis

A

Family history
NSAIDs
Chronic stress and depression

189
Q

What investigations would you carry out in someone with ulcerative colitis

A

Bloods

  • FBC shows low HBC and Increased WCC
  • Increased CPR/ESR
  • Blood cultures

Stools
- Exclude campy, shigella and salmonella

Imaging

  • AXA - megacolon
  • CXR - perforation
  • CT
  • Ba enema
190
Q

What is the management of ulcerative colitis

A

1st line = aminosalicylitate acid (Mesalazine/sulfalazine)

2nd line = Prednisolone

Additional therapies are steroid sparring (Azathioprine and mercaptopurine)

Infliximab and adalimumab

Surgery

191
Q

What is the management for maintaining remission in ulcerative colitis

A

1st line = 5-ASA’s

2nd line = Azathioprine and 6-mercaptourine

3rd line = Infliximab

192
Q

What is the pneumonic for ulcerative colitis (CLOSEUP)

A 
Continuous inflammation 
Limited to colon and rectum 
Only superficial mucosa affected 
Smoking is protective 
Excrete blood and mucus 
Use aminosalicyates 
Primary sclerosing cholangitis
193
Q

What is the surgical management of ulcerative colitis and when is it indicated

A

Surgery indicated when there is toxic megacolon, perforation and haemorrhage or failure to respond to medicine

  • Total/subtotal colectomy
194
Q

What are the risk factors for Crohn’s

A 
Genetic association with mutations in NOD2 gene on chromosome 16
Smoking 
NSAIDs exacerbate 
Family history 
Chronic stresss
195
Q

What is the oral therapy for crohns

A
  1. Illeocaecal = budesonide
  2. prednisolone
  3. Methotrexate
  4. Infliximab
196
Q

What is the supportive therapy for Crohns

A

High fibre diet
Vitamin supplementation
Smoking cessation

197
Q

What is the management for maintaining remission of Crohns

A

1st Azathioprine
2nd methotrexate
3rd Infliximab

198
Q

What is the pneumonic for Crhons

A

NESTs

No blood/mucus 
Entire GIT 
Skip lesions on endoscopy 
Terminal ileum most affected and transmural 
Smoking is a risk factor
199
Q

Give 5 broad causes of malabsorption.

A
  1. Defective intra-luminal digestion.
  2. Insufficient absorptive area.
  3. Lack of digestive enzymes.
  4. Defective epithelial transport.
  5. Lymphatic obstruction.
200
Q

What are the causes of defective intraluminal digestion

A
  1. Pancreatic insufficiency due to pancreatitis or CF. There is a lack of digestive enzymes.
  2. Defective bile secretion due to biliary obstruction (gallstone) or ileal resection.
  3. Bacterial overgrowth.
201
Q

Why can pancreatitis cause malabsorption?

A

Pancreatitis results in pancreatic insufficiency and so a lack of pancreatic digestive enzymes. There is defective intra-luminal digestion which leads to malabsorption.

202
Q

What can cause insufficient absorptive area

A
  1. Coeliac (Villous atrophy and crypt hyperplasia)
  2. Crohn’s - inflammatory damage = cobblestone mucosa
  3. Extensive surface parasitation = Giardia lambda which coat villli so no absorbing
  4. Small intestinal resection or bypass = procedure for morbid obesity/crohns and infarcted small bowel
203
Q

What can cause a lack of digesitive enzymes

A

Lactose intolerance - undigested lactose passes to the colon where it is eaten by bacteria and Co2 is released as wind and diarrhoea

Bacterial overgrowth

204
Q

What can cause defective epithelial transport

A

Abetalipoproteinaemia - deficient lipoprotein transporter

Primary bile acid malabsorption - mutations in bile acid transporter protein

205
Q

What can cause lymphatic obstruction

A

Lymphoma

TB

206
Q

Define malabsorption

A

Failure to fully absorb nutrients because of epithelial destruction due to problem in the lumen meaning food cannot be digested

207
Q

What is the presentation of malabsorption

A

Diarrhoea/Steatorrhea
Wt loss despite normal calorie intake
lethargy
Anaemia despite normal diet

208
Q

What investigations would you carry out in someone with malabsorption

A

Coeliac tests
Stool microscopy
MRI/CT
Small bowel endoscopy

209
Q

Define coeliac disease

A

Common autoimmune condition characterised by heightened immunological response to ingested gluten

210
Q

What is the epidemiology of coeliac

A

Bimodal from infancy to 50-60 years

F>M

increased in Ireland and N.africa

211
Q

Describe the pathophysiology of coeliac disease

A
  1. Gliadin from gluten deaminated by tissue transglutaminase leading to increased immunogenicity
  2. Gliadin recognised by HLA-DQ2 receptor on antigen presenting cells = inflammatory response
  3. Plasma cells produce anti-gliadin leading to T cell cytokine activation
  4. Consequences = villous atrophy an crypt hyperplasia = malabsorption
212
Q

What is the presentation of coeliac disease

A 
Fatigue and weakness 
Carbs 
 - Nausea, vomiting, diarehoea
 - Abdo distension + colic 
 - Flatus 
 - Wt loss 
FAT
 - Steatorrhoea 
 - Hyperoxaluria 
Protein 
- Protein losing enteropathy 
Haematinics 
 - Loss of folate and Fe = anaemia
Lymphoma and carcinoma 
Dermatitis Hepetiformis
213
Q

What are the dermatological presentations of coeliac

A

Dermatitis herpetiformis - symmetrical vesicles especially on the elbows which are very itchy

214
Q

What investigations would you carry out in someone with coeliac

A 
FBC, LFTs, INR
Antibodies 
Anti TTG IgA
Anti Endomysial IgA
Anti gliardin IgG
Stools - exclude giardia 
OGD and duodenal biopsy
 - Crypt hyperplasia
- villous atrophy 
intra-epithelial lymphocytes
215
Q

What antibodies would you see in someone with coeliac

A

Anti-endomysial IgA
Anti tissue transglutaminase IgA
Anti-gliadin IgG

216
Q

What would a duodenal biopsy show n coeliac disease

A

Subtotal villous atrophy
Crypt hyperplasia
Intra-epithelial lymphocytes

217
Q

What is the management of coeliac disease

A

Life long gluten free diet and Dapsone for the dermatitis herpetiformis

218
Q

What are the complications of coeliac disease

A

Osteoporosis

Increased risk of gastrointestinal tumour

219
Q

Describe the pathophysiology of appendicitis

A

Inflammation of the vermiform appendix secondary to a faecolith obstruction with bacterial overgrowth

if the appendix ruptures then infected faecal matter will enter the peritoneum and resulting in peritonitis

220
Q

What are the causes appendicitis

A

Faecolith
Lymphoid hyperplasia
Worms

221
Q

What is the epidemiology of appendicitis

A

10-20 years old

222
Q

What are the symptoms of appendicitis

A

Umbilical pain that moves to the right iliac fossa, nausea, constipation and anorexia

223
Q

What are the signs of appendicitis

A

Tenderness with guarding and rebound
Percussion tenderness
Tachycardia

224
Q

What are the investigations in someone with appendicitis

A

Inflammatory markers (ESR, CRP, WCC)

CT is diagnostic

225
Q

What is the management of appendicitis

A

Surgical appendectomy

Antibiotics

226
Q

What are the complications of appendicitis

A

Ruptured appendix - faecal matter in the peritoneal cavity leading to peritonitis

227
Q

Define gastritis

A

Inflammation of the gastric mucosa

228
Q

What are the 5 things that ca break down the mucin layer in the stomach and cause gastritis

A
  1. mucosal Ischaemia due to atherosclerosis
  2. Increased stomach acid (Stress)
  3. Bile reflux
  4. Alcohol
  5. Aspirin and NSAIDs
  6. Helicobacter pylori
229
Q

Why is helicobacter pylori irritant to the gastric mucosa

A

Secrete urease which splits urea into CO2 and ammonia

Ammonia combines to H+ to form ammonium which is toxic to the gastric mucosa resulting in reduced mucus production

230
Q

What are the symptoms of gastritis

A 
Can be asymptomatic 
Epigastric pain and vomiting 
Anorexia 
Weight loss 
Indigestion 
Abdominal bloating
231
Q

What are the red flag symptoms for gastric cancer

A 
Unexplained weight loss 
anaemia 
Evidence of GI bleed or haematemesis 
Dysphagia 
Upper abdominal mass 
Persistent vomiting
232
Q

What are the investigations for gastritis

A

Endoscopy, biopsy and blood tests

233
Q

What are the investigations for someone with H.pylori

A

Serology - Detect IgG antibodies

C-urea breath test - measures CO2 in breath after ingestion of C-urea

Stool antigen test - immunoassay using monoclonal antibodies for detection of H.pylori

234
Q

What is the management of gastritis

A

Decrease alcohol and smoking and irritating foods

Stop NSAIDs

Ant-acids (Magnesium carbonate) or PPI (Omeprazole or H2 receptor blocker (Nizatidine)

235
Q

What is the anti-h.pylori treatment

A

Triple therapy of 2 antibiotics and a proton pump inhibitor

Amoxicillin, omeprazole and clarithomycin

236
Q

Wha are the complications of gastritis

A

Peptic/duodenal ulcer

237
Q

Define oesophago-gastric varices

A

Varices are a dilated vein which risk ruptures resulting in haemorrhage which can result in a GI bleed (occurs when pressure exceeds 12mmHg)

238
Q

What are the causes of oesophagi-gastric varices

A

Alcoholism and viral cirrhosis
Portal hypertension
1. Pre-hepatic
- Thrombosis in portal or splenic vein

  1. Intra-hepatic
    - Cirrhosis
    - Schistosomiasis
    - Sarcoid
    - Congenital hepatic fibrosis
  2. Post hepatic
    - Budd chiari (Hepatic vein obstruction by tumour or thrombosis)
    - Right heart failure
    - Constrictive pericarditis
239
Q

What is the clinical presentation of oesophagi-gastric varices

A

If ruptured

  • haematemesis
  • Abdominal pain
  • Shock
  • Fresh rectal bleeding
  • Pallor
240
Q

What is the treatment of oesophago-gastric varices

A

IV terlipressen to cause vasoconstriction
Variceal banding
Balloon tamponade

241
Q

What disorders might be associated with coeliac disease

A 
Other autoimmune disorders:
1. T1 diabetes. 
2. Thyroxoicosis. 
3. Hypothyroidism. 
4. Addisons disease. 
Osteoporosis is also commonly seen in people with coeliac disease.
242
Q

What cells normally line the oesophagus?

A

Stratified squamous non-keratinising cells.

243
Q

What is Barrett’s oesophagus?

A

When squamous cells undergo metaplastic changes and become columnar cells.

244
Q

What can cause Barrett’s oesophagus?

A
  1. GORD.
  2. Obesity.
  3. Hiatus hernia
  4. Smoking
245
Q

Give a potential consequence of Barrett’s oesophagus.

A

Adenocarcinoma.

Squamous cell carcinoma

246
Q

Describe how Barrett’s oesophagus can lead to oesophageal adenocarcinoma.

A
  1. GORD damages normal oesophageal squamous cells.
  2. Glandular columnar epithelial cells replace squamous cells (metaplasia).
  3. Continuing reflux leads to dysplastic oesophageal glandular epithelium.
  4. Continuing reflux leads to neoplastic oesophageal glandular epithelium - adenocarcinoma.
247
Q

What are the causes of squamous cell carcinoma int the oesophagus

A

Smoking
Alcohol
Nitrous amines

248
Q

Give 5 symptoms of oesophageal carcinoma.

A
  1. Dysphagia.
  2. Odynophagia (painful swallowing).
    People often present very late.
  3. Vomiting.
  4. Weight loss.
  5. Anaemia.
  6. GI bleed
  7. Reflux
249
Q

Give 3 causes of gastric cancer.

A
  1. Smoked foods.
  2. Pickles.
  3. H.pylori infection.
  4. Pernicious anaemia.
250
Q

Describe how gastric cancer can develop from normal gastric mucosa.

A

Smoked/pickled food diet leads to intestinal metaplasia of the normal gastric mucosa. Several genetic changes lead to dysplasia and then eventually intra-mucosal and invasive carcinoma.

251
Q

What investigations might you do in someone who you suspect to have oesophageal carcinoma?

A

. Barium swallow.
2. Endoscopy.
CT/MRI for staging

252
Q

Describe the 2 treatment options for oesophageal cancer.

A
  1. Medically fit and no metastases = operate. The oesophagus is replaced with stomach or sometimes the colon. The patient often has 2/3 rounds of chemo before surgery.
  2. Medically unfit and metastases = palliative care. Stents can help with dysphagia.
253
Q

Give 3 signs of gastric cancer.

A
  1. Weight loss.
  2. Anaemia.
  3. Vomiting blood.
  4. Melaena.
  5. Dyspepsia.
254
Q

A mutation in what gene can cause familial diffuse gastric cancer?

A

CDH1 - 80% chance of gastric cancer.

Prophylactic gastrectomy is done in these patients.

255
Q

What investigations might you do in someone who you suspect has gastric cancer?

A
  1. Endoscopy.
  2. CT.
  3. Laparoscopy.
256
Q

What is the advantage of doing a laparoscopy in someone with gastric cancer?

A

It can detect metastatic disease that may not be detected on ultrasound/endoscopy.

257
Q

What is the treatment for proximal gastric cancers that have no spread?

A

3 cycles of chemo and then a full gastrectomy. Lymph node removal too.

258
Q

What is the treatment for distal gastric cancers that have no spread?

A

3 cycles of chemo and then a partial gastrectomy if the tumour is causing stenosis or bleeding. Lymph node removal too.

259
Q

What vitamin supplement will a patient need following gastrectomy?

A

They will be deficient in intrinsic factor and so will need vitamin B12 supplements to prevent pernicious anaemia.

260
Q

What is the dukes classification for tumour invasion

A

Dukes’ A: Invasion into but not through the bowel wall
Dukes’ B: Invasion through the bowel wall penetrating the muscle layer but not involving lymph nodes
Dukes’ C: Involvement of lymph nodes
Dukes’ D: Widespread metastases[7]

261
Q

Which one of the following is FALSE regarding colorectal cancer?

a. Bowel cancer screening is offered to people aged 55 or over
b. The majority of cancers occur in the proximal colon
c. FAP and HNPCC are two inherited causes of colon cancer
d. Proximal cancers usually have a worse prognosis
e. Patients with PSC and UC have an increased risk of developing colon cancer

A

b. The majority of cancers occur in the proximal colon

Majority of cancers occur in the distal colon but proximal cancers have worse prognosis

262
Q

A 50 year old man presents with dysphagia. Which one of the following suggests a benign nature of his disease?

a. Weight loss
b. Dysphagia to solids initially then both solids and liquids
c. Dysphagia to solids and liquids occurring from the start
d. Anaemia
e. Recent onset of symptom

A

c. Dysphagia to solids and liquids occurring from the start

If solids then liquids it suggests the lumen is slightly narrowed

263
Q

A 32 year old lady complains of a 6 month history of bloating and diarrhoea. What is the most likely diagnosis based on the small bowel histology?

a. Crohn’s disease
b. Ulcerative colitis
c. Microscopic colitis
d. Coeliac disease
e. Irritable bowel syndrome

A

d. Coeliac disease

264
Q

A 19 year old girl presents with abdominal pain and loose stool. Which of the features suggest that she has irritable bowel syndrome?

a. Anaemia
b. Nocturnal diarrhoea
c. Weight loss
d. Blood in stool
e. Abdominal pain relieved by defaecation

A

e. Abdominal pain relieved by defaecation

265
Q
  1. Which statement is true regarding Helicobacter pylori?
    a. It is a gram-positive bacteria
    b. HP prevalence is similar in developing and developed countries
    c. 15% of patients with a duodenal ulcer are infected with H. Pylori
    d. PPIs should be stopped 1 week before a H. Pylori stool antigen test
    e. It is associated with an increased risk of gastric cancer
A

e. It is associated with an increased risk of gastric cancer

Increased risk of gastric adenocarcinoma, peptic ulcer disease and mucosa associated lymphoid tissue (MALT)

266
Q

A 56 year old man presents with abdominal distension and shortness of breath. Examination revealed fever of 38C, a tense distended abdomen with shifting dullness. He also has dullness to percussion in the right lung base. Several spider naevi are seen on his chest. Which is the most important test in the management of this patient?

a. CXR
b. Ultrasound abdomen
c. Echocardiogram
d. Ascitic tap

A

Ascitic tap

267
Q
  1. Which of the following features best distinguishes Ulcerative colitis from Crohn’s disease?
    a. Ileal involvement
    b. Continuous colonic involvement on endoscopy
    c. Non-caseating granuloma
    d. Transmural inflammation
    e. Perianal disease
A

b. Continuous colonic involvement on endoscopy

268
Q

A 68 year old lady presents with abdominal pain and distention. She last opened her bowels 5 days ago. She has a poor appetite and has lost some weight recently. Her PMH includes an abdominal hysterectomy and diverticulosis. She drinks 20 units of alcohol a week and smokes 5 a day. Examination reveals a distended abdomen with tympanic percussion throughout. There is a small left groin lump with a cough impulse. Which one of the following is NOT likely to be the cause of her abdominal pain and distention?

a. Colon cancer
b. Adhesions
c. Ascites
d. Diverticulitis
e. Strangulated hernia

A

Ascites

269
Q
  1. A patient drinks 4 pints (568ml=1 pint) of beer (4%) a day, and 2 standard (175ml) glasses of red wine (13%) on Saturday and Sunday additionally. How many units of alcohol is he drinking per week? (round up to nearest whole number)
    a. 73 units
    b. 62 units
    c. 94 units
    d. 57 units
    e. 49 units
A

73 units

% x ml / 1000

270
Q
  1. A 71 year old man was admitted to hospital with pneumonia after he returned from a cruise holiday in the Mediterranean Sea. He was treated with a week of augmentin (co-amoxiclav) for his pneumonia. On day 7 of his admission, he started having diarrhoea 10 times a day without any blood. He feels unwell and dehydrated. He had a flexible sigmoidoscopy which showed this. What is the likely organism responsible for his diarrhoea?
    a. Norovirus
    b. Escherichia coli
    c. Giardia lamblia
    d. Clostridium difficile
    e. Salmonella enteritidis
A

Clostridium difficile

271
Q
  1. A 52 year old lady presents with fatigue and itching. She noticed pale stool and dark urine. She suffers from hypercholesterolaemia and rheumatoid arthritis. She takes simvastatin and cocodamol. Examination revealed jaundice, xanthelasma, spider naevi, and hepatomegaly. Her bloods showed Bili 150, ALP 988, ALT 80, positive AMA and a raised IgM. What is the most likely diagnosis?
    a. Simvastatin induced liver injury
    b. Primary biliary cirrhosis
    c. Gall stones
    d. Autoimmune hepatitis
    e. Primary sclerosing cholangitis
A

b. Primary biliary cirrhosis

272
Q
  1. A 16 year old girl is admitted with vomiting and abdominal pain. She reports taking 20 paracetamol tablets after her boyfriend split up with her. Which one of the following test results would you NOT expect to see?
    a. Metabolic acidosis
    b. A prolonged prothrombin time
    c. A raised creatinine
    d. Hyperglycaemia
    e. ALT 1000
A

Hyperglycaemia

Should be hypo because there is an inhibition of gluconeogenesus

Raised creatinine because of renal failure

273
Q
  1. A 68 year old unkempt and malnourished homeless man was brought to the hospital with haematemesis. Endoscopy found bleeding varices. Subsequent USS showed a coarse shrunken liver. On day 2 admission he was found to be ataxic, confused with nystagmus. What is the most likely cause of his neurological presentation?
    a. Alcohol toxicity
    b. Alcohol withdrawal
    c. Delirium tremens
    d. Wernicke’s encephalopathy
    e. Korsakoff syndrome
A

Wernickes Encephalopathy

274
Q

What are the symptoms of alcohol withdrawal

A

occurs 6-24 after last drink, lasts up to a week

• - tremor, insomnia, N+V, agitation, seizures

275
Q

What are the symptoms of delirium tremens

A

most severe form of alcohol withdrawal (5-20%)
• - usually occurs 24 to 72 hours after alcohol cessation
• - hyperadrenergic state, disorientation, tremors, diaphoresis, impaired attention/consciousness, and visual and auditory hallucinations.

276
Q

What are the symptoms of wernickes encephalopathy

A

due to exhaustion of thiamine reserves (malnutrition, alcoholism)
• - triad of : ataxia, nystagmus/ophthalmoplegia, confusion (but only 10% patients have all 3)
• - acute onset, reversible with IV thiamine

277
Q

What are the symptoms of Korsakoff syndrome

A

85% untreated WE leads to Korsakoff syndrome
• - memory impairment, confabulation
• - chronic and irreversible

278
Q
  1. A 23 year old man was brought in at 2am with RIF pain and was diagnosed with acute appendicitis. He was stable and was scheduled for appendicectomy in the morning. During the ward round, he acutely deteriorated. He was immediately brought to theatre for a perforated appendix. What clinical signs would you NOT expect to see?
    a. Fever
    b. Bowel sounds
    c. Tachycardia
    d. Rebound tenderness
    e. Guarding
A

Bowel sounds

279
Q

Anti-DsDNA antibody is associated with what condition

A

SLE

280
Q

The anti-phospholipid antibody is associated with what condition

A

Anti-phospholipid syndrome

281
Q

ANCA antibodies are associated with what condition

A

Small cell vasculitis

282
Q

Alpha gliadin antibody is associated with what condition

A

Coeliac

283
Q

RF antibody is associated with what condition

A

Rheumatoid arthritis

284
Q

Ferrous Sulphate is what sort of drug

A

Iron supplement

285
Q

Loperamide is what sort of drug

A

anti-diarrhoea

286
Q

methotrexate is what sort of drug

A

DMARD

287
Q

Metronidazole is what sort of drug

A

Antibiotic

288
Q
  1. South African patient with Left iliac abdominal region pain and not able to pass stool with no previous surgery, non-smoker and his transglutamase results are negative – what’s the diagnosis
    a. Coeliac disease
    b. Colorectal cancer
    c. Large bowel obstruction – volvus
    d. Small bowel obstruction – adhesion
    e. Strangulation hernia
A

Large bowel obstruction – volvus

289
Q
  1. Which of the following is not a feature of Crohn’s?
    a. Mouth ulcers
    b. Mucosal inflammation
    c. Granulomatous skip lesions
    d. Raised CRP
    e. Smoking decreases level of risk
A

Smoking decreases level of risk

This is true in ulcerative colitis but in Crohn’s smoking increases the risk of disease

290
Q
  1. Symptoms of IBD rather than IBS
    a. Smelly stools
    b. DXA scan revealing decreased bone mineral density
    c. Nocturnal diarrhoea
    d. Abdominal cramps
    e. Feeling fatigued
A

c. Nocturnal diarrhoea

291
Q

Which of the following two statements about ascending cholangitis are false

a. Caused by bacterial infection of biliary tree
b. Patients experience epigastric pain
c. Patients present with a temperature
d. Patients present with yellowing of the skin and sclera
e. Murphy’s sign is negative

A

b. Patients experience epigastric pain
- Should be RUQ pain as ascending cholangitis symptoms are charcots triad
e. Murphy’s sign is negative

292
Q
  1. Gallbladder is supplied by the cystic artery which is a branch of what
    a. Coeliac trunk
    b. Gastroduodenal
    c. Left gastric epiploic
    d. Right hepatic
    e. Splenic
A

Right hepatic

293
Q
  1. Which form of hepatitis is a DNA virus
    a. Hep A – Faeco/oral
    b. Hep B - blood and bodily fluids
    c. Hep C - blood and bodily fluids
    d. Hep D – Blood and bodily fluids
    e. Hep E - Faeco-oral
A

Hep B is DNA, all the others are RNA

294
Q
  1. Haemochromatosis is metabolic liver disease caused by uncontrolled intestinal absorption of what ion
    a. Ca2+
    b. Cu2+
    c. Fe2+
    d. Li+
    e. K+
A

Fe2+

295
Q
  1. Which antibiotics are given alongside PPI for h.pylori and peptic ulcer
    a. Amoxicillin and clarithromycin
    b. Doxycyclin and metronidazole
    c. Ethambutol and trimethoprim
    d. Lithium and clarithromycin
    e. Rifampicin and amoxicillin
A

Amoxicillin and clarithomycin

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