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Phase 2a > GI&L > Flashcards

GI&L Flashcards

1
Q

what is oesophagus lined by?

A

stratified squamous epithelium, which extends
distally to the squamocolumnar junction where the oesophagus joins the
stomach, recognised endoscopically by a zigzag (‘Z’) line, just above the most
proximal gastric folds

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2
Q

what is the lower oesophageal sphincter responsible for?

A

prevention of gastric reflux

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3
Q

GORD epidemiology?

A
  • people who overeat
  • smokers
  • alcohol users
  • pregnancy
  • drugs; antimuscarinics, CCB and nitrates
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4
Q

aetiology of GORD?

A
  • lower oesophageal sphincter hypotension
  • hiatus hernia (80% due to sliding -> where the gastro-oesophageal junction and part of the stomach slide up into chest and 20% rolling -> where the gastro-oesophageal junction remains in abdomen BUT part of fungus prolapses)
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5
Q

pathophysiology of GORD?

A
  • in GORD -> MUCH MORE transient lower oesophageal sphincter
    relaxations as the LOS has reduced tone thereby allowing gastric acid to flow
    back into the oesophagus
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6
Q

clinical presentations of GORD?

A
  • oesophageal -> heartburn, nelching, acid brash and painful swallowing
  • extra-oesophageal -> nocturnal asthma, chronic cough, laryngitis and sinusitis
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7
Q

Ddx of GORD?

A
  • CAD
  • biliary colic
  • peptic ulcer disease
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8
Q

investigations of GORD?

A
  • if there are no alarm bell signs (weigh loss and haemtemesis and dysphagia) then treatment without investigation
  • if alarm bells then endoscopy and barium swallow
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9
Q

treatment for GORD?

A
  • lifestyle changes
  • pharma -> antacids (MAGNESIUM TRISLICATE MIXTURE s/e diarrhoea), alginates (GAVISCON), PPI (LANSOPRAZOLE) and h2 receptor antagonist (CIMETIDINE)
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10
Q

GORD complications?

A
  • peptic stricture (oesophagiitis which narrows the oesophagus -> worsening dysphagia -> treatment endoscopic dilation and long term PPI therapy)
  • Barrets oesophagus (distal oesophageal epithelium metaplasia from squamous to columnar)
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11
Q

what is mallory-weiss tear?

A
  • linear mucosal tear occurring at oesphagogastic junction and produced by sudden increase in intra-abdominal pressure
  • seen after alcoholic dry heaves -> follows counts of coughing or retching
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12
Q

risk factors for mallory-weiss tear?

A
  • alcoholism
  • forceful vomiting
  • eating disorders
  • Male
  • NSAID abuse
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13
Q

clinical features of mallory-weiss tear?

A
  • vomiting
  • haematemesis
  • postural hypotension
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14
Q

investigations and treatment of mallory-weiss tear?

A

endoscopy

most bleeds are minor and heal in 24hrs

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15
Q

dyspepsia?

A

upper abdominal
symptoms such as; heart burn, acidity, epigastric pain or discomfort, fullness or
belching
(postprandial fullness, early satiety and epigastric pain >4 weeks)

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16
Q

clinical presentation of dyspepsia?

A
  • reflux when lying flat
  • heartburn
  • acid taste
  • blowing
  • indigestion
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17
Q

dyspepsia -> cancer?

A

if cancer;

  • unexplained weight loss
  • anaemia
  • evidence of GI bleed
  • dysphagia
  • upper abdominal mass
  • persistant vomiting
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18
Q

management fo dyspepsia?

A
  • dietary review
  • antidepressants- SSROS (CITALOPRAM)
  • endoscopy
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19
Q

stomach layers?

A
  • (outer longitudinal,

inner circular and innermost oblique layers)

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20
Q

duodenum muscle layers?

A

(outer longitudinal and inner smooth muscle)

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21
Q

pariental cells
chief cells
ECL cells?

A

Parietal cells - secrete HCl
• Chief cells - produce pepsinogen and thus initiate proteolysis - the
digestion of proteins
• Enterochromaffin-like (ECL) cells - releases histamine (stimulates acid
release)

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22
Q

what is in antral mucosa?

A
  • Mucus secreting cells - secrete mucin (protects gastric
    mucosa) and BICARBONATE
    • G cells - secrete gastrin which stimulates acid release
    • D cells - secrete somatostatin that is a suppressant of acid
    secretion
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23
Q

prostaglandins in mucosal barrier?

A

Prostaglandins stimulate the secretion of mucus and their synthesis is
INHIBITED by ASPIRIN and NSAIDs, which inhabit cyclo-oxygenase

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24
Q

duodenal mucosa?

A

Has villi like the rest of the small bowel and also contains Brunner’s glands
which secrete alkaline mucus

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25
Q

peptic ulcer disease?

A

break in the superficial epithelial cells penetrating
down to the muscularis mucosa of either the stomach or the duodenum; there is a
fibrous base and an increase in inflammatory cells

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26
Q

most common peptic ulcer?

A

duodenal

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27
Q

peptic ulcer disease, epidemiology?

A
  • elderly
  • developing countries due to H pylori
  • NSAID use
  • decline in incidence in men and now rising in women
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28
Q

aetiology of peptic ulcer disease?

A
  • h pylori
  • NSAIDs
  • increased gastric acid secretion
  • smoking
  • delayed gastric emptying
  • O blood group
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29
Q

pathophysiology of peptic ulcer disease? NSAIDs

A

Ulcers result in gastritis (inflammation of the gastric cells)
- Usually the gastric mucosa is protected by a layer of MUCIN that is produced
by gastric cells
- Mucous secretion is stimulated by prostaglandins (in inflamed tissue,
prostaglandin triggers inflammatory response thus inhibition = less
inflammation)
• Cyclo-oxygenase 1 is needed for prostaglandin synthesis
• NSAIDS inhibit cylclo-oxygenase 1
• Thus reduced mucosal defence

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30
Q

pathophysiology of peptic ulcer disease? H pylori

A

• Highly adapted to the stomach environment and exclusively colonises
gastric epithelium and inhabits the mucous layer or just beneath it
• Causes major destruction to the mucin layer that protects the mucosa
• Causes the decrease in duodenal HCO3- thereby increasing the acidity
of the stomach as there will be less alkali to buffer the acid
• Secretes urease, splitting urea into CO2 and ammonia
• Ammonia + H+ = ammonium
• Ammonium is toxic to gastric mucosa resulting in less mucous produced
• Secreted proteases, phospholipase & vacuolating cytotoxin A can then
begin attacking the gastric epithelium further reducing mucous
production
• Results in an inflammatory response and less mucosal defence
• Also increases gastrin (released from G cells) release thereby causing
more acid secretion from parietal cells and also triggering the release of
histamine which further increases acid secretion
• Also increases parietal cell mass meaning more acid production
• Also decreases somatostatin (released from D cells) release (which
reduced acid secretion) resulting in increased acid release
• Increased acidity overwhelms the protective mucin resulting in mucosal
damage and ulceration

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31
Q

clinical presentations of peptic ulcer disease?

A
  • recurrent burning epigastric pain
  • nausea
  • anorexia and weight loss
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32
Q

complications of ulcers

A
  • duodenal ulcers can go to gasproduodenal artery and cause haemorrhage
  • can cause peritonitis if enters peritoneum
  • can cause acute pancreatis
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33
Q

investigations of peptic ulcer disease?

A
  • <55 yrs -> non-invasive testing eg serological test (tests for IgG antibodies), breath test (C-urea for H pylori) or stool antigen ( uses monoclonal antibodies to test for H pylori)
  • > 55 endoscopy
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34
Q

treatment of peptic ulcer disease?

A
  • lifestyle adjustments
  • stop NSAIDs
  • If h pylori positive; triple therapy ( PPI and METRONIDAZOLE/CLARTIHROMYCIN OR QUONOLONES
  • H2 antagonists -> RANTIDINE
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35
Q

oesophageal gastric varices?

A

A varices is just a dilated vein which is at risk of rupture resulting in haemorrhage
and in the GI system can result in GI bleeding

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36
Q

types of portal hypertension?

A
  • Pre-hepatic; blockage of the hepatic portal vein before the liver
  • Intra-hepatic; distortion of the liver architecture, either pre-sinusoidal (e.g.
    schistosomiasis) or post-sinusoidal (e.g. cirrhosis)
  • Post-hepatic; venous blockage outside the liver (RARE)
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37
Q

epidemiology og oesophageal gastric varicose?

A

Around 90% of patients with CIRRHOSIS will develop gastro-oesophageal
varices over 10 years - but only a third of these will bleed

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38
Q

aetiology of oesophageal gastric varices

A
  • alcoholism and viral cirrhosis
  • preheptaic -> thrombosis in portal or splenic vein
  • intra hepatic -> cirrhosis and schistomiasis
  • post hepatic -> budd-chiari syndrome (tumour or thrombosis obstruction hepatic vein)
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39
Q

pathophysiology of oesophageal gastric varices?

A

Following liver injury and fibrogenesis e.g due to cirrhosis, the contraction
of activated myofibroblasts (mediated by endothelin, nitric oxide and
prostaglandins) contributes to increased resistance to blood flow
- This leads to portal hypertension → splanchnic vasodilation → drop in BP
→ increased cardiac output to compensate for BP → salt and water
retention to increase blood volume and compensate → hyperdynamic
circulation (high circulatory volume)/increased portal flow → Formation of
collaterals between the portal and systemic systems e.g. in the lower oesophagus and gastric cardia → Gastro-oesophageal varices develop one
portal pressure is above 10mmHg and start to bleed i.e. rupture when above
12mmHg - this can occur RAPIDLY and could result in MAJOR
HAEMORRHAGE

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40
Q

clinical presentations of oesophageal gastric varcices?

A
  • signs of chronic liver damage
  • splenomegaly
  • ascites
  • hyponatreamia
  • If ruptured:
    • Haematemesis
    • Abdominal pain
    • Shock - if major blood loss
    • Fresh rectal bleeding - associated with shock in acute massive GI bleed
    • Hypotension and tachycardia
    • Pallor
    • Suspect varices as the cause of GI bleeding if there is alcohol abuse or
    cirrhosis
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41
Q

investigations for oesophageal gastric varices?

A

endoscopy

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42
Q

treatment for oesophageal gastric varices?

A

BLOOD TRANSFUSION aiming to get Hb to 80g/L
- Correct clotting abnormalities - administer VITAMIN K and PLATELET
TRANSFUSION
- Vasopressin - IV TERLIPRESSIN - to cause vasoconstriction, use IV
SOMATOSTATIN if terlipressin is contraindicated e.g. in ischaemic heart
disease
- Variceal banding - where a band is put around varice using an endoscope,
after a few days the banded varix degenerates and falls off leaving a scar
- Ballon tamponade to reduce bleeding by placing pressure on varice if
banding fails
- Transjugular intrahepatic portoclaval shunt (TIPS) - only used when
bleeding cannot be controlled wither acutely or following a rebleed,
essentially a shunt between the systemic and portal systems which reduces
sinusoidal and portal vein pressure

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43
Q

achalasia?

A

difficulties passing food and liquid down oesophagus into stomach

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44
Q

epidemiology of achalasia?

A
  • F=M

- long history of dysphagia

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45
Q

pathophysiology of achalasia?

A

The lower oesophageal sphincter fails to relax due to degeneration of the
mesenteric plexus of the oesophagus with reduction of ganglion cell
numbers

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46
Q

clinical presentation of achalasia?

A
  • dysphagia
  • regurgitation of food at night
  • weight loss
  • spontaneous chest pain
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47
Q

investigations of achalasia?

A
  • CXR
  • barium swallow
  • gold standard-> MANOMETRY -> shows failure of relaxation of lower oesophageal sphincter
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48
Q

treatment of achalasia?

A
  • relief of symptoms -> NIFEDIPINE, NITRATES

- surgery -> endoscopic balloon dilation or botox injections to relax sphincter

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49
Q

SCLERODERMA/SYSTEMIC SCLEROSIS:

A

Scleroderma/Systemic sclerosis is a multi-system disease that affects the
body by hardening connective tissue

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50
Q

Scleroderma/Systemic sclerosis, epidemiology?

A
  • F>M

- 30-50 yrs peak

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51
Q

Scleroderma/Systemic sclerosis, risk factors?

A
  • vinyl chloride

- silica dust

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52
Q

Scleroderma/Systemic sclerosis, pathophysiology?

A
  • Diminished peristalsis and oesophageal clearance due to the replacement
    of the smooth muscle by fibrous tissue
  • Lower oesophageal sphincter pressure is decreased thereby allowing
    GORD with consequent mucosal damage
  • Strictures may develop
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53
Q

clinical presentations, Scleroderma/Systemic sclerosis

A
  • initially no symptoms

- dysphagia

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54
Q

Scleroderma/Systemic sclerosis, investiahtions

A
  • barium swallow - gold standard
  • CXR
  • manometry
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55
Q

gastritis?

A

Gastritis is inflammation that is associated with mucosal injury

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56
Q

aetiology of gastritis?

A
  • H pylori
  • autoimmune
  • Virus
  • reflux
  • Aspirin and NSAIDs
  • alcohol
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57
Q

pathophysiology of gastritis?

A
  • Autoimmune gastritis - affects the fundus and body of the stomach leading to
    atrophic gastritis and loss of parietal cells with intrinsic factor deficiency
    resulting in pernicious anaemia (low RBCs due to low B12)
  • Aspirin and NSAIDs e.g. Naproxen will inhibit prostaglandins (which
    stimulate mucus production) via the inhibition of cyclo-oxygenase resulting in
    less mucus production and thus gastritis
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58
Q

clinical presentations of gastritis?

A
  • nausea
  • abdominal bloating
  • epigastric pain
  • indigestion
  • vomiting
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59
Q

investigations for gastritis?

A
  • endoscopy - gold
  • biopsy
  • Pylori urea and stool test
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60
Q

treatments for gastritis?

A
  • lifestyle change
  • triple therapy; PPI, METRONIDAZOLE/CLARTHROMYCIN and CIPROFLOXACIN
  • h2 antagonist - RANITDINE
  • antacids
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61
Q

diseases that result in malabsorption?

A
  • coeliac
  • tropical sprue
  • crohns
  • parasite infection
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62
Q

causes of malabsorption; defective intraluminal digestion?

A

Pancreatic insufficiency:
- Pancreas produce majority of digestive enzymes such as amylase
(breaks down starch)
- Pancreatitis causes damage to most of the glandular pancreas
meaning less or no enzymes are released
- Cystic fibrosis results in the blockage of the pancreatic duct due to
excess mucus meaning enzymes fail to be released

• Defective bile secretion (lack of fat solubilisation):
- Biliary obstruction e.g. gall stone
- Ileal resection - we reabsorb bile salts in the terminal ileum so if
removed then bile salt reuptake will be decreased

• Bacterial overgrowth

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63
Q

causes of malabsorption; insufficient absorptive area?

A

Essentially anything that damages microvilli and villi thereby reducing
absorptive surface area and thus absorption potential

• Coeliac disease (gluten sensitive enteropathy):
- Villi are very short if present at all, since there is villous atrophy
and crypt hyperplasia
- Lots of lymphocytes in the epithelium

• Crohn’s:
- Causes inflammatory damage to the lining of the bowel resulting in
cobblestone mucosa with significant reduction of absorptive
surface area

• Giardia lamblia:

  • Extensive surface parasitisation of the villi and microvilli
  • Parasites coat the surface of the villi thus food cannot be absorbed

• Surgery - small intestine resection or bypass - in small bowel infarction

Lack of digestive enzymes:
• Disaccharidase deficiency (lactose intolerance) - cannot break down
the lactose in milk into glucose which can then be absorbed. The
undigested lactose passes into the colon where it is then eaten up by
bacteria and CO2 is released leading to wind and diarrhoea

• Bacterial overgrowth resulting in brush border damage
- Defective epithelial transport:
• Abetalipoproteinaemia - lack of transporter protein to transport
lipoprotein across cell
• Primary bile acid malabsorption - mutations in bile acid transporter
protein

  • Lymphatic obstruction:
    • Lymphoma
    • Tuberculosis
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64
Q

what is coeliac disease?

A

Condition in where there is inflammation of the mucosa of the upper small bowel
that improves when gluten is withdrawn from the diet and relapses when gluten is
reintroduced

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65
Q

epidemiology of coeliac disease?

A

Occurs at any age but peaks in infancy and 50-60yrs

  • Affects males and females equally
  • 10% risk in 1st degree relatives and 30% risk in siblings
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66
Q

risk factors for coeliac disease?

A

Other autoimmune diseases since having one will increase risk of others:
• Type 1 diabetes
• Thyroid disease
• Sjorgrens
- IgA deficiency
- Breast feeding
- Age of introduction to gluten into diet
- Rotavirus infection in infancy increases risk

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67
Q

pathophysiology of coeliac disease?

A

In wheat, in gluten the prolamin a-GLIADIN is toxic and resistant to
digestion by pepsin and chymotrypsin because of their high glutamine and
proline content and remain in the intestinal lumen thereby triggering
immune responses

The gliadin peptides pass through the epithelium and are deaminated by
tissue transglutaminase, which increases their immunogenicity
- The gliadin peptides then bind to antigen-presenting cells which interact
with CD4+ T cells in the lamina propria via HLA class II molecules DQ2 or
DQ8

These two HLA class II molecules DQ2 (95%) or DQ8 (5%) ACTIVATE the
gluten-sensitive T cells
- These T cells produce pro-inflammatory cytokines and initiate an
inflammatory cascade
- The cascade releases metaloproteinkinases and other mediators, which
contribute to the VILLOUS ATROPHY, CRYPT HYPERPLASIA and intraepithelial lymphocytes that are typical of the disease and result in
malabsorption
- The mucosa of the PROXIMAL SMALL BOWEL is predominantly affected
- This mucosal damage can mean that B12, folate and iron CANNOT be
absorbed resulting in ANAEMIA

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68
Q

clinical presentations of coeliac disease?

A

1/3 are asymptomatic (silent disease) and only detected on routine blood
tests (raised MCV)
- Stinking stools/fatty stools (steatorrhoea)
- Diarrhoea
- Abdominal pain
- Bloating
- Nausea & vomiting
- Angular stomatitis - inflammation of one or both corners of mouth
- Weight loss
- Fatigue
- Anaemia
- Osteomalacia - softening of bones due to impaired bone metabolism due to lack
of phosphate, calcium and vitamin D leading to OSTEOPOROSIS
- Dermatitis hepetiformis - red raised patches, often with blisters that burst on
scratching, commonly seen on elbows, knees and buttocks

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69
Q

investigations for coeliac disease?

A 
should maintain gluten for at least 6 weeks before testing to get true
results!: 
- FBC; low Hb, B12 and ferritin 
- GOLD STANDARD -> duodenal biopsy 
- serum antibody testing (IgA)
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70
Q

treatment for coeliac disease?

A
  • lifelong gluten free diet

- correction and vitamins and mineral deficiencies

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71
Q

what is tropical sprue?

A 
severe malabsorption (of two or more
substances) accompanied by diarrhoea and malnutrition
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72
Q

epidemiology of tropical sprue?

A

Occurs in residents or visitors to tropical areas where the disease is
endemic; most of Asia, some Caribbean islands, Puerto Rico and parts of
South America

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73
Q

pathophysiology of tropical sprue?

A

Villous atrophy with malabsorption
- Onset is acute and occurs either a few days or many years after being in the
tropics
- Epidemics can break out in villages, affecting thousands of people at the
same time

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74
Q

clinical presentations of tropical sprue?

A

Diarrhoea

  • Anorexia
  • Severe malabsorption
  • Weight loss
  • Abdominal distension
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75
Q

investigation of tropical sprue?

A
  • FBC

- jejunal biopsy - Jejunal mucosa is abnormal showing partial villous atrophy

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76
Q

treatment of tropical sprue?

A

Leave area
- FOLIC ACID daily and antibiotic to ensure complete recovery e.g.
TETRACYCLINE for up to 6 months
- Severe cases require resuscitation with fluids and electrolytes for
dehydration and nutritional deficiencies should be corrected and B12 given

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77
Q

major forms of IBD?

A
  • Ulcerative colitis (UC) - which affects ONLY the COLON

- Crohn’s disease (CD) - can affect ANY PART of the GI tract (mouth-anus)

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78
Q

epidemiology of IBD?

A
  • jewish people more prone?
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79
Q

epidemiology of UC?

A
  • Highest incidence and prevalence in Northern Europe, UK and North
    America
  • M=F
  • more common in non/ex smokers
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80
Q

risk factors of UC?

A
  • family history
  • NSAIDs
  • chronic stress
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81
Q

pathophysiology of UC?

A
  • Begins in the rectum and extends to ileocaecal valve
  • Circumferential and continuous inflammation - NO SKIP LESIONS
    • Mucosa looks reddened and inflamed and bleeds easily (friability)
    • Ulcers and pseudo-polyps (regenerating mucosa) in severe disease
  • no granulotoma
  • depleted goblet cells
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82
Q

clinical presentations of UC?

A
  • LLQ pain
  • episodic or chronic pain with blood/mucus
  • cramps
  • clubbing, oral ulcers and Erythema nodusum
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83
Q

investigations for UC?

A
  • blood test; low Hb, raised WCC and platelets, high ESR and CRP and LFT abnormal
  • pANCA may be positive
  • stool samples
  • faecal calprotein (IBD but not specific)
  • GOLD STANDARD - colonoscopy with mucosal biopsy
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84
Q

treatment for UC?

A 
-5-ASA aminosalicylates are SULFASALAZINE,
MESALAZINE or OLSALAZINE
- glucocorticoid 
- ASA intolertant - AZATHIOPRINE
- surgery
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85
Q

churns disease?

A

chronic inflammatory GI disease characterised by transmural (goes deep into
mucosa) granulomatous inflammation affecting ANY part of the gut from mouth to
anus (especially in TERMINAL ILEUM and PROXIMAL COLON)

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86
Q

epidemiology of chrons?

A
  • Highest incidence and prevalence in Northern Europe, UK and North
    America
  • F>M
  • smoking increases risk
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87
Q

risk factors for chrons?

A
  • stronger genetic association (chr 16)
  • smoking
  • NSAIDs
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88
Q

pathophysiology of chrons?

A

NOT CONTINUOUS i.e. there are SKIP
LESIONS/patchy areas where there is a gap
between affected and unaffected mucosa
• Involved bowel is usually thickened and is often
narrowed
• COBBLESTONE appearance due to ulcers and
fissures in mucosa
• Affect ANY part of GI tract

Inflammation EXTENDS through ALL LAYERS (transmural) of the bowel
• Increase in chronic inflammatory cells and there is lymphoid
hyperplasia
• Granulomas present in 50-60% - these are non-caseating epithelioid cell
aggregates with Langhans’s giant cells
• Goblet cells are present
• Less crypt abscesses’ than UC

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89
Q

clinical presentation?

A
  • weigh loss
  • abdo pain
  • lethargy
  • abdominal mass
  • anal strictures
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90
Q

investigations of chrons?

A
  • examination - tenderness RIGHT ILIAC FOSS
  • bloods; low Hb but no b12
  • raised ESR and WWC
  • NEGATIVE pANCA
  • colonoscopy
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91
Q

treatment of chrons?

A
  • smoking cesstion
  • corticosteroids (mild - BUDESONIDE, moderate PREDNISOLONE and severe IV HYDROCORTISONE)
  • if no improvements, INFLIMAB
  • AZATHIOPRINE or METHOTEXATE given
  • surgery
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92
Q

hirshprungs disease?

A

In neonates they are born without complete innervation of colon to rectum
• Results in gut dilatation and the filling of faeces which remains
since no ganglion cells to result in peristalsis and movement
of contents - resulting in obstruction

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93
Q

adhesions - obstruction?

A

Sticking together of abdominal structures
to one another, bowel loops, omentum,
other solid organs or the abdominal wall
by fibrous tissue
- This is the MOST COMMON CAUSE of
OBSTRUCTION in adults (80%)
Commonly occurs after surgery
- In the intestines, the loops of the small and large intestines can
normally move around freely within the abdominal cavity
- When adhesions form, the intestines are no longer able to mover
around freely because they become tethered to each other, the
abdominal wall or to other abdominal organs
- At the sites where the adhesions occur, the intestine can twist on
itself, resulting in the obstruction of blood supply or the normal
movement of the contents of the intestines - the small intestine in
particular

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94
Q

volvulus?

A
  • A twist/rotation of segment of bowel e.g. sigmoid colon which is
    on a long mesentery can twist on itself resulting in obstruction
  • ALWAYS occurs at the part of bowel with mesentery
  • Type of closed loop bowel obstruction
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95
Q

epidemiology of small bowel obstruction?

A

Accounts for 60-75% of intestinal obstruction

  • Majority is caused by previous surgery (60%)
  • Crohn’s disease is also a significant cause (25%)
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96
Q

aetiology of small bowel obstructions?

A

Adhesions (60% of SBOs):
- Usually secondary to previous abdominal surgery
- Increased incidence in; pelvic, gynaecology and colorectal
surgery

Hernia 
Abnormal protrusion of an organ or tissue out of the body cavity in
which it normally lies
- Particularly in the developing world
- Untreated can result in strangulation

Malignancy
Chrons disease

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97
Q

pathophysiology of small bowel obstruction?

A

Mechanical obstruction is most common e.g. adhesions, hernia and
Crohn’s
- Obstruction of the bowel leads to bowel distension above the block with
increased secretion of fluid into the distended bowel
- Also leads to proximal dilatation, above the block, resulting in:
• Increased secretions and swallowed air in the small bowel
• More dilatation results decreased absorption and mucosal wall oedema
• Increased pressure with the intramural vessels becoming compressed
resulting in ischaemia and or perforation

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98
Q

clinical presentation of small bowel obstruction?

A

Pain - initially colicky (starts and stops abruptly) then diffuse, pain is higher in
the abdomen than in LBO
- Profuse vomiting that follows pain - VOMITING occurs EARLIER in SBO
compared to LBO
- Less distension as compared to LBO (since the more distal the obstruction
the greater the distension)
- increased bowel sounds

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99
Q

investigations for small bowel obstruction?

A
  • GOLD standard - CT
  • Xray
  • FBC
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100
Q

treatment of short bowel obstruction?

A

Aggressive fluid resuscitation

  • Bowel decompression
  • Analgesia and antiemetic
  • Antibiotics
  • Surgery - to remove obstruction done by laparotomy (open surgery)
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101
Q

epidemiology of Large bowel obstruction?

A
  • less common 25%

- africa -> volvulus

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102
Q

pathophysiology of large bowel obstruction?

A

The colon proximal to obstruction dilates
- There is increased colonic pressure and decreased mesenteric blood flow
resulting in mucosal oedema - transudation of fluid and electrolytes from the
lumen
- This can compromise the arterial blood supply and also cause mucosal
ulceration resulting in full thickness necrosis as well as perforation
- Bacterial translocation can also occur resulting in sepsis

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103
Q

presentation large bowel obstruction?

A

Abdominal pain that is more constant than in SBO

  • Abdominal distension
  • Bowel sounds normal then increased then quiet later
  • Palpable mass e.g. hernia, distended bowel loop or caecum
  • Late vomiting which is more faecal like - suggestive of LBO
  • vomiting may be absent tho
  • constipation
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104
Q

investigations of large bowel obstruction?

A
  • DRE
  • FBC
  • Xray
  • CT
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105
Q

treatment of large bowel obstruction?

A

Aggressive fluid resuscitation
- Bowel decompression
- Analgesia and antiemetic
- Antibiotics
- Surgery - to remove obstruction done by laparotomy (open surgery)
• Obstruction due to malignancy required colorectal stents followed by
elective surgery

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106
Q

pseudo-obstruction?

A

Clinical picture mimicking obstruction but with no mechanical cause

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107
Q

pseudo-obsruction, aetiology?

A 
Intra-abdominal trauma
• Pelvic, spinal and femoral fractures
• Postoperative states e.g. abdominal, pelvic, cardiothoracic, orthopaedic
and neuro
• Intra-abdominal sepsis
- pneumonia 
- opiate use
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108
Q

clinical presentation fo pseudo -obstruction

A

Patients present with rapid and progressive abdominal distension and pain

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109
Q

investigation and treatment for pseudo obstruction?

A

X-ray shows a gas-filled large bowel

- treatment -> IV NEOSTIGMINE

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110
Q

types of bowel ischemai?

A

Acute mesenteric ischaemia

  • Chronic mesenteric ischaemia (AKA intestinal angina)
  • Ischaemic colitis (AKA chronic colonic ischaemia)
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111
Q

acute mesenteric ischemia, epidemiology?

A

Usually seen in those over 50

- Almost always involves the small bowel

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112
Q

aetiology of acute mesenteric ischemia?

A

Superior mesenteric artery (SMA) thrombosis - COMMONEST CAUSE
• Superior mesenteric artery (SMA) embolism (e.g. due to AF) - rarer now
• Mesenteric vein thrombosis - common in younger patients with
hypercoagulable states and tends to affect small lengths of bowel
• Non-occlusive disease - occurs in low flow states and reflects poor
cardiac output

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113
Q

clinical presentation fo acute mesenteric ischemia?

A

TRIAD

  • acute - severe abdominal pain
  • rapid hypovolemia -> shock
  • AF (atrial fibrillation)
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114
Q

investigations for acute mesenteric ischemia?

A
  • FBC
  • AXR
  • GOLD STANDARD - laparotomy
  • CT/MRI angiography
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115
Q

treatment for acute mesenteric ischemia?

A

Fluid resuscitation

  • Antibiotics e.g. IV GENTAMICIN & IV METRONIDAZOLE
  • IV HEPARIN to reduce clotting
  • Surgery to remove dead bowel
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116
Q

ischemic colitis?

A

Usually follows low flow in the inferior mesenteric artery (IMA) territory and
ranges from mild ischaemia to gangrenous colitis

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117
Q

epidemiology and risk factors of ischemic colitis?

A
  • elderly
  • underlying atherosclerosis and vessel occlusion

RF

Thrombosis
• Emboli
• Decreased cardiac output and arrhythmias
• Drugs e.g. oestrogen, antihypertensives, vasopressin
• Surgery e.g. cardiac bypass, aortic dissection and repair, aortoiliac
reconstruction
• Vasculitis e.g. SLE, sickle cell disease and polyarthritis nodosa (hep B
& C)
• Coagulation disorders

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118
Q

pathophysiology of ischemic colitis?

A

Occlusion of branched of the superior mesenteric artery (SMA) or inferior
mesenteric artery (IMA), often in the older age group
- The anatomy of the vascular supply to the colon results in a watershed area
at the splenic flexure - which is thus the MOST COMMON SITE AFFECTED

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119
Q

clinical presentation of ischemic colitis

A
  • Sudden onset lower LOWER LEFT SIDE abdominal pain
  • Passage of bright red blood with/without diarrhoea
  • May be signs of shock (pale skin, weak rapid pulse, reduce urine output,
    confusion) and evidence of underlying cardiovascular disease
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120
Q

investigation of ischemic colitis?

A

Urgent CT scan to exclude perforation

  • Flexible sigmoidoscopy:
    • Biopsy shows epithelial cell apoptosis
  • Colonoscopy and biopsy - GOLD STANDARD:
    • Only done AFTER patient has fully recovered to exclude stricture
    formation at the site of disease and confirm mucosal healing
  • Barium enema:
    • Thumb printing of submucosal swelling at splenic flexure
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121
Q

treatment of ischemic colitis?

A

Fluid replacement
- Antibiotics - to reduce infection risks due to translocation of bacteria across
possibly dying gut wall

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122
Q

what is haemorrhoids?

A

Disrupted and dilated anal cushions (masses of spongy VASCULAR (veins
and arteries) tissue due to swollen veins around the anus

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123
Q

epidemiology of haemorrhoids

A
  • 45-65 yrs

- M=F

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124
Q

aetiology of haemorrhoids

A
  • constipation
  • diarrhoea
  • anal intercoruse
  • pregnancy
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125
Q

pathophysiology of haemorrhoids

A

The normal/healthy anus is lined by discontinuous masses of spongy
vascular tissue - the anal cushions, which contribute to anal closure
- They are attached by smooth muscle and elastic tissue but are prone to
displacement and disruption, either singly or together
- The effects of gravity (erect posture), increased anal tone (possibly due to
stress) and the effects of straining when defecating may make them become
both bulky and loose, and so protrude to form piles (from latin, pila - ball)

They are very vulnerable to trauma (e.g. from hard stools) and bleed readily
from the capillaries of the underlying lamina propria
- Since blood loss is from capillaries, it is bright red
- Since there are no sensory fibres above the
dentate line (squamomucosal junction), piles are
not painful unless they thrombus when they
protrude and are gripped by the anal
sphincter, blocking venous return
- There is a vicious circle; the vascular cushions
protrude through a tight anus → become more congested and
hypertrophy → protrude again more readily

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126
Q

classification of haemorrhoids?

A

INTERNAL
1st - Remain in rectum
- 2nd - Prolapse through the anus on defecation but spontaneously
reduce
- 3rd - Prolapse but can be reduced manually
- 4th - Remain persistently prolapsed
EXTERNAL
- originate below dentate line so painful as they protrude

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127
Q

treatment for haemorrhoids

A
  • 1st degree - increase fluid, fibre and stool softener
  • 2/3rd degree - rubber band litigation or infra-red coagulation
  • 4th degree - excision haemorrhoidectomy
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128
Q

what is anal fistula?

A

An abnormal connection between the epithelised surface of the
anal canal and skin - essentially a track communicates between
the skin and anal canal/rectum

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129
Q

aetiology of anal fistula?

A 
Perianal sepsis
• Abscesses
• Crohn’s
• TB
• Diverticular disease
• Rectal carcinoma
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130
Q

clinical presentation of anal fistula?

A
  • pain
  • discharge
  • Pruritus ani (itchy bottom)
  • Systemic abscess if it becomes infected
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131
Q

investigation of anal fistula?

A
  • MRI

- endoanal US

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132
Q

treatment of anal fistula?

A

Surgical - Fistulotomy and excision

- Drain abscess with antibiotics if infected

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133
Q

anal fissure?

A

Painful tear in the sensitive skin-lined lower anal canal, distal to the dentate line
resulting in pain on defecation

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134
Q

epidemiology and aetiology of anal fissure?

A
  • F>M

- cause; hard faeces, syphilis, herpes, trauma, chrons

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135
Q

investigation of anal fissure?

A
  • perianal inspection
136
Q

treatment for anal fissure?

A

Increase dietary fibre and fluids to make stools softer

  • LIDOCAINE OINTMENT + GTN OINTMENT or topical DILTIAZEM
  • BOTULINUM TOXIN (botox) INJECTION (2nd line)
137
Q

perianal access? epidemiology, presentation, diagnosis and treatment?

A

Epidemiology:
- 2/3 times more common in gay sex and in those who have anal sex

• Clinical presentation:

  • Painful swellings
  • Tender
  • Discharge

• Diagnosis:

  • MRI
  • Endoanal ultrasound

• Treatment:

  • Surgical excision
  • Drainage with antibiotics
138
Q

pilonidal sinus/abcess?

A

Hair follicles get stuck under the skin in the natal cleft (butt crack) resulting in
irritation and inflammation leading to small tracts which can become infected
(abscess)

139
Q

epidemiology of pilonidal sinus?

A

Much more common in MALES than females

- Commonly presents between 20-30 yrs

140
Q

risk factors of pilonidal sinus?

A

Obese caucasians and those from Asia, Middle East and Mediterranean are
at increased risk
- Large amount of body hair
- Sedentary job
- Occupation involving sitting or driving
- Family history

141
Q

treatment of pilonidal sinus?

A

Surgery:
• Excision of the sinus tract and primary closure and pus drainage
• Pre-op antibiotics
- Hygiene and hair removal advice (near sinus)

142
Q

IBS?

A

mixed group of abdominal symptoms for which no organic cause can
be found

143
Q

IBS epidemiology?

A

Age of onset is under 40

  • More common in FEMALES than males
  • Common, in western world
144
Q

aetiology of IBS?

A 
Depression, anxiety
• Psychological stress and trauma
• GI infection
• Sexual, physical or verbal abuse
• Eating disorders
145
Q

types of IBS?

A
  • IBS-C - with constipation
  • IBS-D - with diarrhoea
  • IBS-M - with constipation and diarrhoea
146
Q

pathophysiology of IBS?

A

Dysfunction in the brain-gut axis results in
disorder of intestinal motility and or
enhanced visceral perception (visceral
hypersensitivity)

147
Q

clinical presentation of IBS?

A 
Painful period
• Urinary frequency, urgency, nocturia and incomplete emptying of
bladder
• Back pain
• Joint hypermobility
• Fatigue

ABC
abdominal pain, bloating and change in bowel habit

148
Q

investigations of IBS?

A

ruling out!

  • FBC
  • ESR and CRP
  • EMA and tTg test
  • faecal calprotectin
  • colonoscopy
149
Q

treatment for IBS?

A
  • lifestyle and diet changes
  • soluble fibre is good, insoluble makes it worse
  • LOW FODMAP DIET
  • antispasmodics eg MEBEVERINE
  • laxatives MAVICOL/SENNA
  • anti-motility LOPERAMIDE
  • tricyclic antidepressants AMITRIPTYLINE
150
Q

diverticular disease and diverticulitis definitions?

A

Diverticulosis = presence of diverticula
• Diverticular disease = diverticula are symptomatic
• Diverticulitis = inflammation of a diverticulum

151
Q

epidemiology of diverticular disease?

A
  • > 50 yrs

- sigmoid colon most frequent

152
Q

aetiology of diverticular disease?

A 
Low fibre diet:
- Commonly eaten in developed countries
- Rare in rural Africa
• Obesity
• Smoking
• NSAIDs
153
Q

pathophysiology of diverticula

A

Diverticular forms at gaps in the wall of the gut where blood vessels
penetrate
• In a low fibre diet, the colon must push harder to move things along
(fibre helps gut motility) so pressure increases
• This pressure increase results in pouches of mucosa being extruded
through the muscular wall through weakened areas near blood vessels
leading to diverticula formation
• There is also thickening of the muscle layer

154
Q

pathophysiology of acute diverticulitis

A

Occurs when faeces obstruct the neck of the diverticulum, causing
stagnation and allowing bacteria to multiply and produce inflammation
• This can then lead to bowel perforation (peridiverticulitis), abscess
formation, fistulae into adjacent organs, haemorrhage and generalised
acute peritonitis and possibly death

155
Q

clinical presentation of diverticular disease?

A

Asymptomatic in 95% of cases and is usually detected incidentally on
colonoscopy or barium enema examination

• In symptomatic cases:

  • Intermittent left iliac fossa pain
  • Erratic bowel habit

• In severe cases:
- Severe pain and constipation due to luminal narrowing

156
Q

acute diverticulitis clinical presentation?

A
  • severe pain LEFT ILIAC FOSSA
  • fever
  • constipation
  • tachycardia
157
Q

complications of diverticular disease

A
  • perforation
  • fistula formation
  • intestinal obstruction
  • bleeding
  • mucosal inflammation
158
Q

investigation for diverticular disease and acute diverticulitis

A 
diverticular disease 
- COLONOSCOPY
acute diverticulitis
- ESR and CRP raised
- gold standard CT COLONOGRAPY
159
Q

diverticular disease treatment?

A

In uncomplicated symptomatic disease recommend a well-balanced
HIGH FIBRE DIET with smooth muscle relaxants i.e. antispasmodics
e.g. MEBEVERINE

160
Q

acute diverticulitis treatment

A

Mild attacks can be treated with oral antibiotics e.g. CIPROFLOXACIN
and METRONIDAZOLE
• Those with signs of systemic upset (fevers, tachycardia) and significant
abdominal pain require bowel rest, IV fluids and IV antibiotics
• Surgical resection is occasionally required

161
Q

merkel diverticulum?

A

Most common congenital abnormality of the GI tract
• Affects 2-3% population

Acute inflammation of the diverticulum also occurs and is indistinguishable
clinically from acute appendicitis
• Treatment is surgical removal of diverticula, often laparoscopically (keyhole)

162
Q

acute appendicitis, where is it?

A

Located at McBurney’s point which lies 2/3 of the way
from the umbilicus to the Anterior Superior Iliac
Spine (ASIS)

163
Q

epidemiology of appendicitis?

A

More common in MALES than females
- Can occur at any age although highest incidence is
between 10-20 yrs
- Rare before age of 2 since appendix is cone shaped with a larger lumen

164
Q

pathophysiology of appendicitis

A

Occurs when the lumen of the appendix becomes obstructed by lymphoid
hyperplasia, filarial worms or a FAECOLITH (most common) resulting in the
invasion of gut organisms into the appendix wall
- This leads to oedema, ischaemia, necrosis and perforation as well as
INFLAMMATION
- If the appendix ruptures then infected and faecal matter will enter the
peritoneum resulting in life threatening peritonitis

165
Q

clinical presentation of appendicitis

A
  • pain moves from epigastrium to right iliac fossa
  • anorexia
  • pyrexia
  • nausea and vomiting
166
Q

investigations for appendicitis

A
  • blood tests; raised WCC, CRP &ESR
  • USS
  • CT - GOLD STANDARD
167
Q

treatment for appendicitis

A
  • surgery

- IV antibiotic pre-op eg IV METRONIDAZOLE

168
Q

acute pancreatitis, aetiology?

A

I GET SMASHED

I - idiopathic 
G - gallstones (60%)
E - ethanol (30%)
T - trauma 
S- steroids 
M - mumps
A - autoimmune
S - scorpion venom
H - hyperlipidemia 
E- ERCP
D- drugs (diuretics, ACE inhibitors)
169
Q

pathophysiology of acute pancreatitis?

A

Acute pancreatitis is caused by the destructive effect of premature
activation of pancreatic enzymes which causes self-perpetuating pancreatic
inflammation by enzyme-mediated AUTOdigestion

The prematurely activate enzymes also cause leaky vessels by digesting
vessel walls in the pancreas leading to the leakage of fluid into the tissues
causing OEDEMA, INFLAMMATION and HYPOVOLAEMIA

Destruction of blood vessels by enzymes causes haemorrhage
- Destruction of the adjacent islets of Langerhans can result in
hyperglycaemia as beta cells will be destroyed resulting in less insulin

170
Q

gallstone pancreatitis pathophysiology?

A

Accumulation of enzyme-rich fluid WITHIN the pancreas due to
OBSTRUCTION of the pancreatic duct by gallstones
• Intracellular Ca2+ increases and causes the early activation of
trypsinogen
• In this situation, trypsinogen is cleaved (by cathepsin B) to trypsin, and
trypsin degradation (by chymotrypsin C) is impaired and overwhelmed
leading to a buildup of trypsin and thus increased enzymatic digestion
of the pancreas and inflammation leading to extensive acinar damage

171
Q

alcohol induced pancreatitis pathophysiology?

A

Alcohol is shown to interfere with Ca2+ homeostasis in increased
stimulation of enzyme secretion and obstruction of the duct due to
contraction of the ampulla of Vater

172
Q

clinical presentation of acute pancreatitis?

A

Gradual or sudden severe epigastric or central abdominal pain that radiates
to the back - sitting forward may relieve
- Anorexia, nausea and vomiting
- Tachycardia
- Fever
- Jaundice
- hypotension
- Periumbilical ecchymosis (skin discolouration due to
blood under skin due to bruising) - Cullen’s sign
- Left flank bruising (skin discolouration due to blood
under skin due to bruising) - Grey Turner’s sign

173
Q

investigation for acute pancreatitis?

A
  • blood test; serum amylase raised, urinaru amylase raised, CRP raised, serum lipase raised
  • XCR
  • AUSS
  • CT
  • MRI
174
Q

treatment for pancreatitis?

A
  • analgesia
  • Prophylactic antibiotics like beta-lactams e.g CEFUROXIME or another type
    e. g. METRONIDAZOLE to reduce risk of infected pancreatic necrosis
175
Q

chronic pancreatitis?

A

Debilitating continuing inflammatory process of the pancreas resulting in
progressive loss of exocrine pancreatic tissue which is replaced with by fibrosis

176
Q

chronic pancreatitis, epidemiology?

A
  • M>F
  • alcohol use
  • CKD
  • hereditary
177
Q

pathophysiology of chronic pancreatitis?

A

Obstruction or reduction in bicarbonate secretion, which produces an
alkaline pH which in turn stabilises trypsinogen, leads to the activation of
trypsinogen as pH rises making it more unstable and causing its activation
into trypsin which leads to pancreatic tissue necrosis with eventual fibrosis

178
Q

clinical presentation of chronic pancreatitis?

A
  • epigastric pain that goes to the back
  • nausea and vomiting
  • exocrine dysfunction
  • exocrine dysfunction
179
Q

investigations for chronic pancreatitis?

A
  • serum amylase and lipase may be elevated but not in advanced disease
  • AUSS and contrast CT - GOLD STANDARD
180
Q

treatment of chronic pancreatitis?

A
  • alcohol sessation
  • NSAIDs, opiates and trycylci antidepressants
  • duct drainage
  • PPI
181
Q

autoimmune chronic pancreatitis?

A

Chronic pancreatic inflammation which results from an autoimmune process

• High prevalence in Japan

• Presentation is very similar to normal chronic pancreatitis
• There are elevated levels of serum gammaglobulins and immunoglobulin G (IgG)
levels - IgG4
• Autoantibodies such as antinuclear cytoplasmic antibody (ANCA) and
rheumatoid factor may also be elevated

• This condition is steroid responsive with glucocorticoid therapy e.g. ORAL
PREDNISOLONE for 4-6 weeks

182
Q

presentation of acute liver injury?

A
  • malaise
  • nausea
  • anorexia
  • maybe jaundice
183
Q

presentation of chronic liver injury?

A
  • ascites
  • oedema
  • haematemesis
  • bruising
  • hepatomegaly
184
Q

what is serum albumin?

A

Marker of synthetic function and is useful for gauging the severity of
chronic liver disease: a falling serum albumin is a bad prognostic sign
• In acute liver disease, initial albumin levels may be normal

185
Q

bilirubin test?

A
  • Is normally all CONJUGATED
    • In liver disease, increased serum bilirubin is usually accompanied by
    other abnormalities in liver biochemistry
186
Q

AST?

A

Also present in heart, muscle, kidney and brain
• High levels are seen in hepatic necrosis, myocardial
infarction, muscle injury and congestive cardiac failure

187
Q

ALT?

A

More specific to the liver

• A rise only occurs with liver disease

188
Q

Alkaline phospahte test?

A

Present in liver but also in bone, intestine and placenta
- Raised in both intrahepatic and extrahepatic cholestatic disease
of any cause, due to increased synthesis
- Raised levels also occur with heaptic infiltrations (e.g. metastases)
and in cirrhosis

189
Q

bilirubin and haem catabolism?

A

When the erythrocytes is ingested it is broken down into haem and globin

globin is broken down into amino acids and then used to generate new RBC in bone marrow

haem further broken down into biliverdin and fe2+

biliverdin is reduced to UNCONJUGATED bilirubin (BILIVERDIN REDUCTASE). this is toxic and insoluble so transported bound to ALBUMIN to liver

In liver it undergoes glucuronidation to make is soliaable using UDP GLUCURONYL TRANSFERASE -> CONJUGATED bilirubin

CONJUGATED bilirubin travels to small intestine to ileum where by intestinal bacteria it is reduced to UROBILINOGEN

UROBILINOGEN is lipid soluble so 10% reabsorbed into blood and bound to albumin to the liver (can go to the kidney where it is excreted, causing yellow urine)

remaining 90% of UROBILINOGEN is oxidised by different intestinal bacteria to form STERCOBILIN -> faeces to make it brown

190
Q

types of jaundice?

A

PRE HEPATIC
unconjugated
- gilberts syndrome - UDP GLUCURONYL TRANSFERASE deficiency
- haemolysis

HEPATIC
conjugated 
- liver disease 
- hepatitis 
- ischemia

POST HEPATIC

  • gallstones
  • stricture
  • blocked stent
191
Q

what is biliary colic?

A

The term used for the pain associated with the temporary obstruction of the
cystic or common bile duct by a stone migrating from the gall bladder
- The pain of stone-induced ductular obstruction is of sudden onset, severe
but constant and has a crescendo characteristic

192
Q

epidemiology of gallstones?

A
  • > 30 yrs
  • F>M
  • more common with Scandinavians
  • obese
193
Q

risk factors for gallstones?

A

Female

  • Fat
  • Fertile - more kids = increased risk of gallstones
  • Smoking
194
Q

pathophysiology of gallstones?

A

CHOLESTEROL AND BILE PIGMENT

CHOLESTEROL STONE
- formed due to cholesterol crystallisation in bile

BILE PIGMENT STONES

  • mainly formed of ca2+
  • main cause is haemolysis
  • two types black ( calcium bilirubinate seen in haemolytic anaemia) and brown (calcium salts seen in bile stasis)
195
Q

clinical presentation of gallstones?

A
  • most asymptomatic
  • celiac pain
  • start off epigastric pain and then RUQ pain
  • biliary celiac has no fever and jaundice
  • acute cholecystisis has no jaundice
  • cholangitis has jaundice, RUQ pain and fever
196
Q

investigations of gallstones?

A
  • biliary colic - AUSS

- acute cholecystitis - AUSS and blood tests and examination

197
Q

treatment of gallstones?

A
  • laparoscopic cholecystectomy
  • opiates
  • IV antibiotics - CEFTRIAXONE
  • stone dissolution using ORAL URSODEXOYCHOLIC ACID
  • shock wave lithotripsy
198
Q

stone in common bile duct and acceding cholangitis, aetiology?

A
  • common bile duct obstruction by gallstones
  • benign biliary strictures following surgery
  • cancer of head of pancreas
199
Q

ascending chlangitis treatment?

A
  • IV antibiotics

- ERCP - biliary drainage

200
Q

acute v chronic hepatitis?

A

Acute hepatitis is defined as hepatitis within 6 months of onset
• Chronic hepatitis is defined an any hepatitis lasting for 6 months or longer

201
Q

acute hepatitis clinical presentations and investigations?

A
  • general malaise
  • myalgia
  • RUQ pain
  • raised AAST, ALP and bilirubin
202
Q

causes of acute hepatitis?

A
  • Viral - HEP A & E, herpes
  • non viral; Coxiella
  • alcohol, drugs, pregnancy
203
Q

chronic hepatitis clinical presentations and investigation?

A
  • clubbing
  • palmar erythema
  • dupuytren contracture
  • spider naevi
  • LFTs can be normal
204
Q

causes of chronic hepatitis?

A
  • HEP B&C

- alcohol, drugs, autoimmune

205
Q

HEP A, epidemiology?

A
  • most common acute in world
  • endemic in Africa and South America
  • children and young adults
  • contaminated food/water
206
Q

spread of HEP A?

A

Spread via the faeco-oral route

207
Q

risk factors of HEP A?

A

Shellfish

  • Travellers
  • Food handlers
208
Q

pathophysiology of hEP A?

A

Hep A is a picornavirus

  • Replicates in the liver, is excreted in bile and then excreted in the faeces for
    about 2 weeks before the onset of clinical illness and for up to 7 days after
  • Disease is maximally infectious JUST BEFORE the onset of jaundice
  • Short incubation period of 2-6 weeks
  • Causes ACUTE HEPATITIS ONLY
  • Usually is self-limiting (3-6 weeks) - very rarely causes fulminant hepatitis
    (rapid liver injury that can quickly cause liver failure)
  • 100% immunity after infection
209
Q

clinical presentation of HEP A?

A
  • nausea, fever and malaise

- 1-2 weeks -> jaundice (dark urine and pale stools)

210
Q

investigations of HEP A?

A 
before jaundice 
- serum bilirubin will be normal 
- raised AST or ALT
after jaundice
- serum bilirubin will rise
  • blood test (LOW WCC & RAISED ESR)
  • viral markers (HAV antibodies and IgM)
211
Q

treatment for HEP A??

A
  • supportive treatment
  • avoid alcohol
  • manage close contacts
    PREVENTION!! - good hygiene and immunisation
212
Q

HEP E, epidemiology?

A
  • older men
  • common in UK
  • self limiting
213
Q

HEP E, transmission route?

A

Faeco-oral route of transmission - water or food-borne

214
Q

HEP B, epidemiology?

A
  • present world wide

- endemic in Far East and Africa

215
Q

HEP B, transmission route?

A
  • blood borne -> needle stick, sex, mother -> child
216
Q

risk factors for HEP B?

A

Healthcare personnel

  • Emergency and rescue teams
  • CKD/dialysis patients
  • Travellers
  • Homosexual men
  • IV drug users
217
Q

pathophysiology of HEP B?

A
  • DNA virus
  • The complete virus comprises of an inner core or nucleocapsid surrounded by
    an outer envelope of surface protein (Hepatitis B surface antigen (HBsAg))

HBsAg is produced in excess by the infected hepatocytes and can exist
separately from the whole virus in serum and body fluid
- After penetration into hepatocyte the virus loses its coat and the virus core
is transported to the nucleus without processing
- Following infection, which may be subclinical (i.e. little symptoms), around
1-10% of patients will not clear the virus and will develop chronic Hep B

Around 1-5% will develop chronic
infection which can lead to cirrhosis and
then decompensated cirrhosis and then
liver failure

Both cirrhosis and chronic infection
can lead to HEPATOCELLULAR
CARCINOMA - VERY BAD

218
Q

clinical presentations of HEP B?

A
  • nausea, fever, malaise
  • rash
  • 1-2 weeks - jaundice
  • heptaospleomegaly
219
Q

investigations of HEP B?

A

HBsAg is present 1-6 months after exposure

  • HBsAg presence for more than 6 months implies carrier status
  • Anti-HBs - antibodies to hepatitis B
  • IgG
220
Q

treatment for HEP B?

A
  • supportive
  • avoid alochol

CHRONIC

  • SC PEGYLATED INTERFERON-ALPHA 2A:
  • oral TENOFOVIR - nucleotide analogues that inhibit viral replication
221
Q

HEP D, epidemiology?

A

common in eastern Europe

222
Q

HEP D, transmission?

A

blood borne

223
Q

pathophysiology of HEP D?

A

Hepatitis D virus is an incomplete RNA particle enclosed in a shell of Hep B
surface antigen (HBsAg)
- Virus is UNABLE to REPLICATE ON ITS OWN but is activated by the
presence of HBV
- If acquired simultaneously with HBV (co-infection) causes increased severity
of acute infection
- Can either occur as co-infection or superinfection

co infection

  • infection of HBV and HBD
  • has IGM for D and B

superinfection

  • when a person who has chronic HBV gets HBV
  • raised AST or ALT
224
Q

treatment for HEP D?

A

SC PEGYLATED INTERFERON-ALPHA 2A:

225
Q

HEP C, epidemiology?

A
  • Egypt
  • IV drug users
  • rare vertical transmission
226
Q

HEP C, transmission?

A

blood and blood products

227
Q

pathophysiology of HEP C?

A

RNA flavivirus
- 7 genotypes; genotype 1a and 1b account for 70% cases in USA and 50% in
Europe
- Rapid mutations so envelope proteins change rapidly so its hard to develop
a vaccine
- Can result in chronic hepatitis and thus risk of HEPATOCELLULAR
CARCINOMA

228
Q

clinical presentation of HEP C?

A
  • 70% have chronic infection can lead to cirrhosis or liver failure and hepatocellular carcinoma
229
Q

investigations of HEP C?

A
  • HCV antibody (4-6 weeks)

- HCV RNA

230
Q

treatment for HEP C?

A

SC PEGYLATED INTERFERON-ALPHA
2A/B + ORAL RIBAVIRIN

triple therapy of direct acting anti-virals
eg, LEDIPASVIR + SOFOSBUVIR + ORAL RIBAVIRIN

expensive!

231
Q

cirrhosis?

A

it is an end stage of all progressive chronic liver
diseases; which once fully developed is irreversible and may be associated
clinically with symptoms and signs of liver failure and portal hypertension

232
Q

causes of cirrhosis?

A
  • chronic alcohol abuse
  • NAFLD
  • hep B + D
  • hep c
  • hertitary haemochormatosis
  • Wilsons disease
  • alpha anti-tripsin deficiency
233
Q

pathophysiology of cirrhosis?

A

Chronic liver injury results in inflammation, matrix
deposition, necrosis and angiogenesis all of
which lead to FIBROSIS

Liver injury causes necrosis and apoptosis, releasing cell contents and
reactive oxygen species (ROS)
- This activates hepatic stellate cells and tissue macrophages (Kupffer cells)

cells release cytokines that attract neutrophils and macrophages to
the liver which results in further inflammation and thus necrosis and eventual
fibrosis

234
Q

types of cirrhosis regression?

A

Micronodular cirrhosis:
- Regenerating nodules are usually < 3mm in size with uniform
involvement of the liver
- Often caused by alcohol or biliary tract disease

• Macronodular cirrhosis:
- There nodules are of varying size and normal acini (functioning unit
of liver) may be seen within the larger nodules
- Often caused by chronic viral hepatitis

235
Q

clinical presentation of cirrhosis?

A
  • clubbing
  • palmar erythema
  • Dupuytren’s contracture
  • spider naiava
  • abdo pain
  • oedema
  • hepatomegaly
236
Q

investigations of cirrhosis?

A
  • GOLD STANDARD - liver biopsy
  • LFTs (low serum albumin and high PPT)
  • raised AST and ALT
  • Alpha-fetoprotein is highly suggestive of HEPATOCELLULAR CARCINOMA
  • child-pugh SCORE -> looks for ascites, encephalopathy, high bilirubin, low albumin and long PTT
237
Q

complications of cirrhosis?

A

Coagulopathy; fall in clotting factors II,VII, IX & X
• Encephalopathy - liver flap (asterixes - flapping tremor with wrist
extended) & confusion/coma
• Hypoalbuminaemia resulting in oedema
• Portal hypertension:
- Ascites
- Oesophageal varices

238
Q

treatment of cirrhosis?

A
  • half yearly USS screening
  • avoid NSAIDs
  • reduce salt intake
  • liver transplant
239
Q

portal hypertension, main causes?

A

PRE HEAPTIC
portal vein thrombosis

INTRA HEPATIC
cirrhosis
schistomaiasis
sarcocodosis

POST HEPATIC
RHF
IVC obstruction

240
Q

clinical presentations of portal hypertension?

A

Patients are often asymptomatic
- Only clinical sign being splenomegaly which is unspecific
Haematemesis and melaena from ruptured gastro-oesophageal varice
or portal hypertensive gastropathy
-

241
Q

initial management of VARICEAL HAEMORRHAGE:

A

Resuscitate until haemodynamically stable

  • If anaemic then BLOOD TRANSFUSION aiming to get Hb to 80g/L
  • Correct clotting abnormalities - administer VITAMIN K and PLATELET
    TRANSFUSION
  • Vasopressin - IV TERLIPRESSIN - to cause vasoconstriction, use IV
    SOMATOSTATIN if terlipressin is contraindicated e.g. in ischaemic heart
    disease
  • Prophylactic antibiotics to treat and prevent infection as well as reduce
    early rebleeding and mortality e.g. CEPHALOSPORIN
  • Variceal banding - where a band is put around varice using an endoscope,
    after a few days the banded varix degenerates and falls off leaving a scar
  • Ballon tamponade to reduce bleeding by placing pressure on varice if
    banding fails
242
Q

primary biliary cirrhosis? epidemiology?

A
  • F>M
  • 40-50 yrs
  • immunological
243
Q

risk factors for primary biliary cirrhosis?

A

Positive family history

  • Many UTIs
  • Smoking
  • Past pregnancy
  • Other autoimmune disease
  • Use of nail polish/hair dye
244
Q

pathophysiology, primary biliary cirrhosis?

A

Interlobar bile ducts are damaged by CHRONIC AUTOIMMUNE
GRANULOMATOUS INFLAMMATION resulting in cholestasis which may lead
to fibrosis, cirrhosis and portal hypertension
- Serum anti-mitochondrial antibodies (AMA) found in almost all patients
- Likely than an environmental factor acts on genetically predisposed hosts
to trigger disease

245
Q

clinical presentation of primary biliary cirrhosis?

A
  • itchy (pruitus) early symptom
  • lethargy and fatigue
  • jaundice and hepatomegaly
  • xanthelasma - yellow fat deposit on eyelid
246
Q

investigation of primary biliary cirrhosis?

A
  • raised alkaline phosphate
  • raised serum cholesterol
  • Igm and AMA postive
  • USS
  • liver biopsy
247
Q

treatment for primary biliary cirrhosis?

A

URSODEOXYCHOLIC ACID:

COLESTYRAMINE works for itch but unpalatable
• NALOXONE and NALTREXONE (opioid antagonists) shown to help

248
Q

alcoholic liver disease, aetiology?

A

ALCOHOL
genetics
immunological mechanisms

249
Q

pathophysiology for fatty alcoholic liver disease?

A

Metabolism of alcohol produces fat in the liver
• This is minimal with small amounts of alcohol, but with larger amounts
the cells become swollen with fat (steatosis)
• There is no liver cell damage
• The fat disappears on stopping alcohol
• In some cases, collagen is laid down around the central hepatic veins
and this can sometimes progress to cirrhosis without a preceding
hepatitis

• Alcohol directly affects stellate cells, transforming them into collagen-
producing myofibroblast cells

250
Q

pathophysiology of alcoholic hepatitis liver disease?

A

infiltration by polymorphonuclear
leucocytes and hepatocyte necrosis
• Dense cytoplasmic inclusions called Mallory bodies are sometimes
seen in hepatocytes and giant mitochondria are also a feature
• If alcohol consumption continues, alcoholic hepatitis can progress to
cirrhosis

251
Q

pathophysiology of alcoholic cirrhosis liver disease?

A

Classically of the MICRONODULAR TYPE but mixed pattern is also seen
accompanying fatty change, and evidence of pre-existing alcoholic
hepatitis may be present

252
Q

clinical presentation of alcoholic liver disease

A

FATTY
no specific signs or symptoms - mainly nausea, diarrhoea and heptaomegaly

ALCOHOLIC HEP
can be mild jaundice and signs of chronic liver disease (ascites, bruising and clubbing) or severe with jaundice

CIRRHOIS
presents as well with few symptoms

253
Q

investigations of alcoholic liver disease?

A

FATTY

  • raised ALT and AST
  • gold standard USS or CT

ALCOHOLIC HEP

  • leucocytosis
  • raised bilirubin, AST, ALT and PTT

CIRRHOSIS
- liver biopsy

254
Q

treatment for alcoholic liver disease

A
  • stop alcohol
  • IV THIAMINE to prevent Wernicke-Korsakoff encephalopathy
  • reduce salt intake
  • healthy diet
255
Q

paracetamol poisoning

A

Large amounts of paracetamol are metabolised by oxidation because of
saturation of the sulphate conjugation pathway (Phase II reaction)
- Liver GLUTATHIONE stores become depleted so that the liver is unable to
conjugate and activate NAPQI (TOXIC)
- This results in hepatotoxicity as well as paracetamol-induced kidney injury

256
Q

clinical features of paracetamol poisoning?

A
  • Metabolic acidosis
  • HYPOglycaemia (since overdose will inhibit glucose production
    (gluconeogenesis) )
  • Prolonged prothrombin time
  • Raised creatinine
257
Q

treatment of paracetamol poisoning?

A

Gastric decontamination - ACTIVATED CHARCOAL
- Give IV N-ACETYLCYSTEINE which acts by replenishing cellular glutathione
stores (s/e rash)

258
Q

hereditary haemochromatosis?

A
  • Inherited disorder of iron metabolism in which there is increased intestinal
    iron absorption leads to iron deposition in joints, liver, heart, pancreas,
    pituitary, adrenals and skin
259
Q

epidemiology of hereditary haemochromatosis?

A
  • Caucasians

- M>F

260
Q

aetiology of hereditary haemochromatosis?

A

HFE gene mutation on chromosome 6, this is an AUTOSOMAL
RECESSIVE gene (i.e. sufferer must be homozygous) - MOST COMMON
CAUSE

• There are other gene mutations responsible and one is AUTOSOMAL
DOMINANT - but not as common, but means sufferer can be
heterozygous

  • High intake of iron and chelating agents (e.g. ascorbic acid)
  • Alcoholics may have iron overload
261
Q

pathophysiology of hereditary haemochromatosis?

A

The HFE gene protein interacts with the transferrin receptor 1, which is a
mediator in intestinal iron absorption

  • Iron is taken up by the mucosal cells of the small intestine inappropriately,
    EXCEEDING the binding capacity of transferrin
  • Hepcidin, a protein synthesise in the liver, is central to the control of iron
    absorption; it is increased in iron deficiency states and decreased with iron
    overload
  • Hepatic expression of the hepcidin gene is decreased in HFE
    haemochromatosis thereby facilitating iron overload
  • Excess iron is then gradually taken up by the liver and other tissue over a long
    period
  • The iron content is particularly increased in the liver and pancreas but also
    in other organs e.g. heart, skin and endocrine glands
  • In established cases, the
    liver shows extensive iron deposition and fibrosis
  • Cirrhosis is a late feature
262
Q

clinical presentation of hereditary haemochromotosis?

A
  • tiredness and joint pain
  • hypogonadism
  • slate grey appearance, signs of chronic liver disease and osteoporosis
  • later -> bronze skin pigment
263
Q

investigations of hereditary heamatochromosis?

A
  • raised serum iron, ferritin
  • genetic tests
  • liver biopsy
  • MRI
264
Q

treatment for hereditary heamtochromosis?

A
  • venesection
  • testosterone replacement
  • iron low diet
  • avoid food high in vit C
265
Q

Wilsons disease?

A

Rare inherited disorder of biliary copper excretion with too much copper in
the liver and CNS (basal ganglia i.e. globus pallidus and putamen)

266
Q

epidemiology of Wilsons disease?

A
  • More common in caucasians than in Indians and Asians

- autosomal recessive chr 13

267
Q

pathophysiology of Wilsons disease?

A

Dietary copper is normally absorbed from the stomach and upper small
intestine

  • Copper is transported to the liver loosely bound to albumin
  • Once in the liver it is incorporated into a glycoprotein called
    CAERULOPLASMIN synthesised in the liver and secreted into the blood
  • The remaining copper is normally excreted in the bile and excreted in faeces
  • Wilson’s disease is a very rare inborn error of copper metabolism that
    results in copper deposition in various organs, including the liver, the basal
    ganglia of the brain and the cornea
268
Q

clinical presentation of Wilsons disease?

A
  • children - hepatic problems
  • young adults - CNS problems - terror, dysphagia, dyskinesia
  • kaiser-fleischer ring - green/brown pigment in eye caused by copper
269
Q

Wilsons disease, investigations?

A

Serum copper and caeruloplasmin are usually reduced but can be normal
- 24 hour urinary copper excretion is high
- Liver biopsy shows increased hepatic copper, hepatitis and cirrhosis - but
note high copper levels are also found in chronic cholestasis

270
Q

treatment for Wilsons disease?

A

Avoid foods that are high in copper e.g. liver, chocolate, nuts, mushrooms
and shellfish
- Lifelong chelating agent e.g. PENICILLAMINE used to chelate copper

271
Q

alpha 1 anti-tripsin deficiency? epidemiology

A
  • Caucasians
  • family history chr 14
  • autosomal recessive
272
Q

alpha anti-trypsin deficiency, pathophysiology?

A

Alpha-1-antitrypsin is produced in the liver and its main role is to inhibit the
proteolytic enzyme - NEUTROPHIL ELASTASE

  • In the lung, alpha-1-antitrypsin protects against tissue damage from
    neutrophil elastase - a process that is also induced by smoking
  • Deficiency results in:
    • Emphysema
    • Liver cirrhosis
    • Hepatocellular carcinoma
273
Q

alpha antitrypsin deficiency, clinical presentation

A
  • children present with liver disease

- adults present with respiratory problems

274
Q

investigations and treatment for alpha anti trypsin deficiency?

A

investigations
Serum alpha-1-antitrypsin levels are LOW

treatment
there is non by stop smoking and manage liver and lungs

275
Q

hepatic encephalopathy

A

As the liver fails, nitrogenous waste e.g. ammonia builds up in the
circulation and passes to the brain which can result in permanent
brain damage as ammonia is neurotoxic to the brain since it halts
the Krebs cycle resulting in IRREPARABLE CELL DAMAGE and
neural cell DEATH

Also as astrocytes try to clear ammonia (using a process involving
the conversion of glutamate to glutamine), the excess glutamine
causes an osmotic imbalance and a shift of fluid into these cells -
hence cerebral oedema - resulting in damage

276
Q

ascites?

A

accumulation of free fluid within the peritoneal cavity

277
Q

epidemiology of ascites?

A
  • post op

- high sodium diet

278
Q

aetiology of ascites?

A
  • local inflammation
  • low protein
  • low flow due to clots
279
Q

clinical presentation of ascites?

A
  • listened abdomen
  • mild abdo pain
  • respiratory distress
280
Q

investigations of ascites?

A
  • diagnostic aspiration of 10-20ml using ascitic tap

protein measurement of ascitic fluid from ascitic tap

281
Q

treatment for ascites?

A
  • reduce sodium
  • diuretic - ORAL SPIROLACTONE
  • drain fluid
  • TIPS shunts
282
Q

peritonitis?

A

The inflammation of the peritoneum

283
Q

peritonitis, aetiology?

A
  • bacterial

- chemical; bile, old clotted blood

284
Q

clinical presentation of peritonitis?

A

perforation = sudden onset which causes severe abdominal pain and shock/collapse

poorly localised pain which moves to one pint and becomes localised

patients feel better lying still

285
Q

investigations of peritonitis?

A
  • blood tests raised WCC and CRP
  • HCG to exclude pregnancy
  • AXRY and CT scan
286
Q

treatment of peritonitis?

A
  • antibiotics

- surgery

287
Q

types of oesophageal tutors?

A

Squamous cell carcinoma occurs in the middle third (40% of all
oesophageal cancer) and in the upper third (15%) of the
oesophagus
• Adenocarcinomas occur in the lower third of the oesophagus and at
the cardia and represent around 45% of tumours

288
Q

oesophagus squamous cell carcinoma, epidemiology and aetiology?

A

epidemiology

  • middle and upper 3rd
  • M>F

causes

  • high levels of alcohol consumption
  • achalasia
  • smoking
  • obesity
289
Q

pesphagus adenocarcinoma epidemiology and aetiology?

A 
epidemiology 
- lower 3rd
-
causes
- barrets oesphagus 
- gORD
- smoking 
- obesity
290
Q

clinical presentation of oesophageal cancer?

A
  • no physical signs
  • progressive dysphagia (dysphasia to solids and liquids from the start = benign)
  • weigh loss
  • lymphadenopathy
  • anorexia
  • hoarseness and cough
291
Q

diagnosis of oesophageal cancer?

A
  • gold standard; oesphagoscopy with biopsy
  • barium swallow
  • CT scans and PET to se metastases
292
Q

treatment of oesophageal cancer?

A
  • surgical resection with combined chemotherapy and or radiotherapy
293
Q

benign oesophageal tumours, aetiology?

A
  • barrets oesophagus
  • GORD
  • obesity
294
Q

pathophysiology of benign oesophageal tumours?

A

Leiomyomas are smooth muscle tumours arising from the oesophageal wall

  • They are intact, well encapsulated and are within the overlying mucosa
  • Slow growing
295
Q

clinical features of benign oesophageal tumours?

A

Usually asymptomatic, found incidentally on barium swallow

  • Dysphagia
  • Retrosternal pain
  • Food regurgitation
  • Recurrent chest infections
296
Q

investigations and treatment of benign oesophageal tumour?

A

Endoscopy

  • Barium swallow
  • Biopsy to rule out malignancy

treatment
- endoscopic removal or surgical removal

297
Q

gastric adenocarcinoma, epidemiology?

A
  • M>F

- peak age 50-70

298
Q

aetiology of gastric adenocarcinoma?

A
  • smoking
  • H, pylori
  • diet (high salt and nitrates)
  • loss of p53
  • family history
  • pernicious anaemia
299
Q

pathophysiology of gastric adenocarcinoma?

A

Helicobacter pylori infection:
• Normal gastric mucosa → H.pylori infection → ACUTE GASTRITIS →
Chronic active gastritis → Atrophic gastritis → Intestinal metaplasia →
DYSPLASIA → ADVANCED GASTRIC CANCER

2 types;
Intestinal (type 1):
- Well formed and differentiated glandular structures
- distal stomach involved

diffuse (type 2)

Poorly cohesive undifferentiated cells

  • Tend to infiltrate the gastric wall
  • Can involve any part of the stomach, especially the cardia
  • Has a worse prognosis than intestinal
300
Q

clinical presentation of gastric adenocarcinoma?

A
  • epigastric pain
  • nausea and anorexia
  • vomiting
  • dysphagia
  • anaemia
  • palpable lymph node
301
Q

gastric adenocarcinoma investigations?

A
  • gastroscopy and biopsy’s GOLD STANDARD
  • endoscopy
  • CT/MRI/PET
302
Q

treatment of gastric adenocarcinoma?

A
  • nutritional support

- surgery and combined chemotherapy ECF (EPIRUBICIN + CISPLATIN + 5- FLUOROURACIL)

303
Q

small intestinal tumours, risk factors?

A
  • coeliac disease

- crohns disease

304
Q

small intestinal tumour types?

A

Adenocarcinoma is the most common tumour of the small intestine,
accepting for up to 50% of primary tumours

Lymphomas (Non-Hodgkin’s type) are most frequently found in the ileum
and are less common than adenocarcinomas

305
Q

clinical presentation of small intestine tumours?

A

Pain, diarrhoea, anorexia, weight loss, anaemia

- May be a palpable mass

306
Q

small intestine tumour investigations and treatment?

A
  • endoscopic biopsy GOLD STANDARD
  • CT scan

treatment
- surgery and radiotherapy

307
Q

colon polyps?

A

abnormal growth of tissue projecting from the colonic

mucosa

308
Q

types of inherited polyps?

A

Familial adenomatous polyposis (FAP):
• Autosomal dominant condition arising from a mutation in the APC gene
• Characterised by the presence of hundreds to thousands of colorectal
and duodenal adenomas
• Develop adenomas at 16 and cancer develops at 39
• Often given prophylactic colectomy and ileorectal anastamosis

  • Lynch syndrome (Hereditary Non-Polyposis Colon Cancer (HNPCC)):
    • Polyps are formed in the colon and may rapidly progress to colon
    cancer
    • Autosomal dominant condition caused by a mutation in one of the DNA
    mismatch repair genes, usually hMSH2 or hMSH1
    • These genes are responsible for maintaining the stability of DNA during
    replication - this defect causes naturally occurring, highly repeated,
    short DNA sequences known as micro satellites that are shorter or
    longer than normal
    • This increases the risk of DNA damage in replication and thus colorectal
    carcinoma development
    • Thus instead of taking 10-15 years for polyps to develop into colorectal
    carcinoma it occurs more rapidly
309
Q

colorectal carcinoma, epidemiology?

A

Usually ADENOCARCINOMA

  • Majority occur in DISTAL COLON
  • Majority of presentations are in those over 60 yrs
  • M>F
310
Q

risk factors of colorectal carcinoma?

A
  • low fibre diet
  • sugar
  • polyps
  • alcohol and smoking
  • obesity
  • UC
  • increasing age
  • genetic
311
Q

pathophysiology of colorectal cancer?

A

Normal epithelium → Adenoma → Colorectal adenocarcinoma

Polypoid mass with ulceration
- Spreads by direct infiltration through the bowel wall then spread to
lymphatic and blood vessels and metastasis to LIVER and LUNG

312
Q

clinical presentation of colorectal cancer?

A
  • RIGHT SIDED
  • asymptomatic
  • mass
  • weigh loss
  • low Hb

LEFT SIDED

  • change in bowel habits
  • diarrhoea
  • constipation
  • blood in stools

RECTAL
- blood in stools

313
Q

investigations for colorectal cancer?

A

colonoscopy GOLD STANDARD

  • feacal occult blood
  • barium enema
  • CT colonoscopy
  • MRI
314
Q

treatment of colorectal cancer?

A
  • surgery

- endoscopic stenting radiotherapy & chemo

315
Q

liver tumours, epidemiology?

A

Common in China

- More common in MALES than females

316
Q

risk factors of liver tumours?

A

Carriers of HBV and HCV (higher risk) have an extremely high risk of
developing HCC
- Associated with cirrhosis such as alcohol cirrhosis, non-alcoholic fatty liver
disease and haemochromatosis

317
Q

pathophysiology of liver tumours?

A

Tumour is either single or occurs as multiple nodules throughout the liver
- Consists of cells resembling hepatocytes
- It can metastasise via the heaptic or portal veins to the lymph nodes, bones
and lungs

318
Q

INVESTIGATION OF LIVER TUMOURS?

A
  • liver biopsy GOLD STANDARD
  • CT
  • USS
319
Q

treatment of liver tumours?

A
  • surgery

- liver transplant

320
Q

cholangiocarcinoma, epidemiology and risk factors?

A

Epidemiology:

  • Cancer of the biliary tree
  • Responsible for 10% of liver primaries

• Risk Factors:
- Associated with infestation with parasitic worms (flukes) e.g. Clonorchis
sinensis
- Biliary cysts
- Inflammatory bowel disease e.g. UC and Crohn’s

321
Q

clinical presentation and treatment of cholangiocarcinoma?

A

clinical presentation

  • Fever
  • Abdominal pain +/- ascites
  • Malaise
  • Raised bilirubin - jaundice
  • Raised alkaline phosphate

Treatment:

  • Surgical resection is rarely possible and patients die within 6 months
  • Liver transplant is contraindicated
322
Q

secondary liver tumour, clinical presentation

A

Variable

  • Weight loss
  • Malaise
  • Upper abdominal pain
  • Hepatomegaly with/without jaundice
323
Q

investigation and treatment of secondary liver your?

A

Diagnosis:
- Ultrasound is primary investigation with CT or MRI to define metastases and
look for a primary
- Serum alkaline phosphatase is raised

Treatment:

  • Depends on site of the primary and the burden of liver metastases
  • Removal of primary tumour and hepatic resection
  • Chemotherapy is used, particularly with breast cancer
324
Q

pancreatic andemocarcinoma, epidemiology?

A
  • 99% is exocrine
  • M>F
  • > 60 yrs
325
Q

risk factors for pancreatic adenocarcinoma?

A
  • smoking
  • alcohol and coffee
  • aspirin
  • diabetes
  • family history
326
Q

pathophysiology, pancreatic adenocarcinoma?

A
  • starts at ductal epithelium
  • metastasise early
  • 60% in head, 25% in body and 15% in tail
327
Q

clinical presentation of pancreatic adenocarcinoma?

A 
Weight loss
- Diabetes
- Acute pancreatitis
- Head of pancreas:
• PAINLESS obstructive jaundice - pale stools
and dark urine
- Body and tail of pancreas:
• Epigastric pain that radiates to the back and is
relieved by sitting forward
328
Q

investigations of pancreatic adenocarcinoma?

A
  • transabdominal US and CT to find pancreatic mass

- BIOPSY

329
Q

treatment for pancreatic adenocarcinoma?

A
  • surgery

- palliative therapy

330
Q

bacterial abscess aetiology?

A
  • unknown
  • elderly = biliary sepsis
  • trauma
  • bacteria -> e.coli most common
331
Q

bacterial abscess clinical presentation?

A
  • fever
  • vomiting
  • weigh loss
  • RUQ pain
332
Q

investigations of bacterial abscess?

A
  • blood culture
  • Alkaline phosphatase, ESR and CRP raised
  • CT and USS
333
Q

treatment of bacterial abscess?

A
  • aspirate

- antibiotics - CO-AMOXICALV

334
Q

amoebic abscess investigations and treatment?

A

Cyst aspiration shows ‘anchovy sauce pus’ - DIAGNOSTIC

treatment is METRONIDAZOLE for 10 days

335
Q

infective diarrhoea, aetiology?

A

VIRAL

  • children - rotavirus
  • adults - Nora virus and campylobacter

BACTERIA

  • children - e.coli, salmonella and shingllla
  • antibiotic associated ( C antibiotics; CLINDAMYCLIN, CO-AMOXICLA, CEPHALOSPORINS) -> c.diff (treatment is METRONIDAZOLE AND ORAL VANCOMYCIN)

PARASITE
- giardia lamblia

336
Q

investigations of diarrhoea?

A

BLOODS
Low MCV and or Fe deficiency e.g. coeliac disease or colon cancer

High MCV if alcohol abuse or decreased B12 absorption e.g. coeliac
disease or Crohn’s

raised WCC if parasites
Raised ESR and CRP indicate infection, Crohn’s, UC or cancer

  • Stools:
    • Stool culture if suspect bacteria, parasites or C.diff toxin
  • Sigmoidoscopy with biopsy
337
Q

treatment of diarrhoea?

A

Anti-emetics - treat vomiting e.g. METOCLOPRAMIDE

  • Antibiotics
  • Anti-motility agents e.g LOPERAMIDE HYDROCHLORIDE

Phase 2a (12 decks)

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