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Phase 2a > GI > Flashcards

GI Flashcards

1
Q

What is a Mallory Weiss tear and how is it caused?

A

alcoholic binging&raquo_space; retching and vomiting&raquo_space; tear in OG junction&raquo_space; heavy bleeding&raquo_space; haematemesis

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2
Q

Where does a Mallory Weiss tear occur?

A

Oesophageal lining at the oesophageal-gastric junction

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3
Q

How is an acute upper GI bleed (UGIB) assessed?

A

Rockall Score used to assess mortality of acute UGIB

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4
Q

What is dyspepsia?

A

Non specific upper GI abdominal symptoms including discomfort, reflux, indigestion, heartburn, acid taste, N&V and those in the ROME 3 Criteria

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5
Q

What are the causes of dyspepsia?

A 
Excess acid production
Malignancy
GORD
PUD
Drugs
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6
Q

How is dyspepsia classified?

A

ROME 3 Criteria:

  1. post prandial fullness (following meal)
  2. early satiety (unusual fullness after little food)
  3. epigastric pain/burning
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7
Q

What do alarm features (red flags) in dyspepsia mean? and name 5 red flag symptoms…

A

Malignancy

  1. Iron deficiency anaemia
  2. unintentional weight loss
  3. persistent vomiting
  4. epigastric mass
  5. chronic GI bleed
  6. Over 55 years with unexplained and persistent dyspepsia
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8
Q

What investigations should be done in dysphagia and when?

A
  1. epigastric pain + alarm symptoms OR >55yrs = gastroscopy and CLO test (confirms H-pylori)
  2. epigastric pain + NO alarm symptoms AN <55yrs = lifestyle advice / PPI (1 month) / test and treat
  3. if predominantly heart burn treat as GORD
  4. if fun/non-ulcer dyspepsia = lifestyle and diet review, TCA or SSRI
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9
Q

What are the causes of peptic ulcer disease?

A

H-pylori
NSAIDs or Aspirin
Co-administration of corticosteroids and NSAID’s

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10
Q

How does peptic ulcer disease present?

A
  • burning epigastric pain
  • pain relieved by antacids
  • pain when hungry and at night
  • nausea
  • heartburn
  • flatulence
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11
Q

Epigastric pain worse when hungry and at night signifies what condition?

A

Peptic ulcer disease

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12
Q

What is the pre-endoscopic and post-endoscopic management of peptic ulcer disease?

A

Pre-endoscopic:
- Glasgow-Blatchford score = can patient be safely discharged?

Post-endoscopic:
- Rockall’s score and Forrest Classification

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13
Q

What does Rockall’s Score measure?

A

Risk of mortality after an acute upper GI bleed

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14
Q

What does the Glasgow-Blatchford score measure?

A

which patients with an UGIB are safe for discharge

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15
Q

What does the Forrest Classification measure?

A

classifies patients on endoscopic findings into high risk and low risk for intervention

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16
Q

If after endoscopy patients are high risk for intervention what treatment is given?

A

H-pylori test and eradication- IV PPI infusion for 72 hours

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17
Q

If after endoscopy patients are low risk for intervention what treatment is given?

A

H-pylori test and eradication- Oral PPI + discharge

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18
Q

How is PUD treated if H-pylori positive?

A

Triple therapy = 1 PPI and 2 antibiotics for 7 days
- omeprazole + metronidazole + clarithromycin (BD)
OR omperazole + amoxicillin + clarithromycin

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19
Q

When would amoxicillin be used instead of metronidazole and vice versa for PUD if H-pyrlori +ve?

A

If a patient has been treated with metronidazole for other infections amoxicillin and clarithromycin is preferred.

If a patient has been treated with a macrolide for other infections amoxicillin and metronidazole is preferred.

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20
Q

When should ulcers be re-scoped?

A

Within 6-12 weeks to look for malignancy or non-healing

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21
Q

How is PUD treated if H-pylori negative?

A

Use PPI and H2 receptor antagonist

- omeprazole/lansoprazole + ranitidine

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22
Q

What time of day should a PPI and H2RA be given?

A 
PPI = before meals (BD)
H2RA = before bed
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23
Q

What are the complications associated with PUD?

A
  1. peritonitis- PU can erode through muscular layer&raquo_space; leak contents into peritoneum
  2. pancreatitis- can erode back wall of duodenum&raquo_space; erode into pancreas
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24
Q

How do you test for H-pylori?

A

CLO test
- campylobacter-like organism test

H-pylori releases urease enzymes that convert urea into ammonia and CO2
Biopsy taken from antrum of stomach and cultures on medium with urea and phenol red.
Colour change = yellow (-ve) to red (+ve) due to increase pH

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25
Q

Who is most at risk of developing GI complications with an NSAID?

A
  • > 65 years old
  • history of PUD / severe GI complication
  • those taking NSAID’s or aspirin
  • those with severe co-morbidities (CV disease, DM or hepatic or renal impairment)
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26
Q

If PUD is due to NSAID use what is the first think you should do during treatment?

A

Withdraw the NSAID!!!!

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27
Q

When testing for H-pylori how does the CLO test change if patient is on a PPI?

A

Biopsy should be taken from fungus and body (PPIs cause H-pylori to move more proximally in stomach)

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28
Q

What can reduce the accuracy of H-pylori test?

A

An active GI bleed

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29
Q

Why do NSAIDs cause PUD?

A

inhibit cox enzyme and prevent prostaglandin production. Leaves gastric mucosa susceptible to damage as mucus and bicarb are not secreted

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30
Q

Where do gastric ulcers usually form?

A

lesser curvature of stomach

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31
Q

What is Zollinger-Ellison syndrome and what GI disease can it cause?

A

A gastronoma (tumour) in duodenal wall which secretes increased amounts of gastrin. Can cause PUD.

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32
Q

In duodenal ulcers what are you likely to see in the mucosa under the microscope?

A
  • Brunner gland hypertrophy (increase in size in attempt to produce more mucus to protect the damaged area)
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33
Q

How does epigastric pain differ between gastric and duodenal ulcers?

A

Gastric ulcers = increased pain whilst eating (often leads to weight loss)
Duodenal ulcers = decreased pain whist eating (often leads to weight gain)

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34
Q

What substances can worsen peptic ulcers?

A 
NSAIDs
Alcohol
Tobacco
Caffeine
Therefore stop using these ASAP if suspect PUD
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35
Q

What is the blood supply to the liver?

A

Portal vein = 75% of hepatic vascular inflow

Hepatic artery = 25%

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36
Q

How is the portal vein formed?

A

Union of SMA and splenic vein

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37
Q

What is normal portal pressure?

A

5-8mmHg

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38
Q

What is the pathophysiology of oesophageal varices?

A

cirrhosis of liver&raquo_space; scar tissue&raquo_space; impedes blood flow&raquo_space; blood shunted into portosystemic collaterals&raquo_space; veins dilate&raquo_space; veins weak and rupture due to increased pressure

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39
Q

What is the main complication of oesophageal varices?

A

massive haemorrhage

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40
Q

How do oesophageal varices present?

A

splenomegaly and clinical signs of chronic liver disease

  • GI bleeding&raquo_space; haematemesis/melena and abdopain
  • ascites
  • dysphagia
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41
Q

What are the investigations for oesophageal varices?

A

URGENT gastroscopy (rules out bleed from other sites)

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42
Q

What is the management for oesophageal varices?

A

Pre endoscopy- IV Terlipressin (restricts portal inflow by constricting splanchnic arteries)
Endoscopic therpay = band ligation or sclerotherapy
TIPS- forms shunt between portal and hepatic veins to decrease portal P.
Oral propanolol- to prevent recurrent bleeding or primary prophylaxis for varices that have never bled

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43
Q

What is the main cause of oesophageal varices?

A

Cirrhosis which causes portal hypertension

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44
Q

What does TIPS stand for?

A

Transjugular intrahepatic portosystemic shunting

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45
Q

What is the mechanism of action of propranolol in oesophageal varices?

A

lowers resting pulse by 25% to lower portal pressure

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46
Q

What is sclerotherapy and when is it used?

A

Used in gastro-oesophageal varices.
Injection of a sclerosis agent&raquo_space; collapse of vessel
e.g. ethanolamine

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47
Q

Define gastritis

A

inflammation of the stomach lining

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48
Q

Define gastropathy

A

injury to the mucosa of the stomach (associated with cell damage and regeneration)

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49
Q

What are the causes of gastritis?

A

Mainly H-pylori

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50
Q

What are the causes of gastropathy?

A

NSAIDS or aspirin, Crohns, sarcoidosis, CMV, HSV

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51
Q

What is the pathophysiology of gastritis?

A

Stomach usually protected by a layer or mucin but this will break down if…

  1. mucosal ischaemia
  2. increased acid production (H-pylori, stress, aspirin)
  3. bile reflux due to increase alcohol conc
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52
Q

What are the symptoms of gastritis?

A

Usually asymptomatic

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53
Q

What are the symptoms of gastropathy?

A

Indigestion, vomiting, haemorrhage

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54
Q

What is the treatment of gastropathy?

A

PPI

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55
Q

What are the complications associated with an anterior and posterior gastroduodenal ulcer?

A

Anterior = perforates&raquo_space; peritonitis

Posterior&raquo_space; pancreas&raquo_space; pancreatitis

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56
Q

Define GORD

A

chronic condition of mucosal damage where there is reflux of gastric contents (gastric acid) into the oesophagus

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57
Q

What is the incidence of GORD?

A

Affects ~30% of the population

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58
Q

What is the pathophysiology of GORD?

A

Several mechanisms by which GORD can occur:

  1. LOS tone reduced&raquo_space; increased mucosal sensitivity to gastric acid & reduced oesophageal acid clearance
  2. delayed gastric emptying
  3. delayed gastric/oesophageal clearance (gastritis)
  4. hiatus hernia&raquo_space; mechanical aberration
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59
Q

What are the causes of GORD?

A
  • hiatus hernia
  • foods e.g. fat, caffeine, chocolate (relaxes LOS)
  • obesity and pregnancy (increase intra-abdominal P.)
  • smoking
  • systemic sclerosis
  • certain drugs (nitrates and tricyclics)
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60
Q

What are the clinical features of GORD?

A
  • GORD induced dyspepsia
  • regurgitation
  • odynophagia (painful swallowing of solids > liquids)
  • chronic cough
  • dysphagia
  • nocturnal asthma
  • waterbrash (salivation due to presence of acid in oesophagus)
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61
Q

How is GORD diagnosed?

A

Often clinical and no investigations (alway case in those <45yrs and no red flags)

  • OGD if new onset heartburn + RED FLAGS
  • 24hr luminal pH monitoring and manometry
62
Q

What is a positive result for luminal pH monitoring and what does it allow you to rule out?

A

+ve if pH <4 for 6-7% of the 24 hours

Allows you to rule out possibility of oesophageal dysmotility

63
Q

What is the management for GORD?

A

1st line = conservative measures with lifestyle changes + simple antacids
2nd line = PPIs or pro kinetic agents or H2RA
Failure to respond to above = surgery = nissan fundoplication

64
Q

What is a nissan fundoplication?

A

Surgical procedure in which the funds of the stomach is wrapped around the lower oesophagus to produce an anti reflux valve

65
Q

What are two complications associated with GORD?

A
  1. Barrett’s Oesophagus- Squamous to columnar epithelium

2. Oesophageal strictures ‘Schatzki ring’ due to fibrosis&raquo_space; haemorrhage bleeding

66
Q

Name a pro kinetic agent

A

Domperidone

67
Q

Name a H2RA

A

Ranitidine

68
Q

What is an OGD?

A

Oesophago-gastro-duodenoscopy

69
Q

Name two simple antacids and their side effects

A
  1. magnesium tricilicate- diarrhoea

2. aluminium hydroxide- constipation

70
Q

What is a pro kinetic agent and give an example…

A

Enhances GI motility by increasing freq or strength of contractions in small intestine (DOES NOT DISRUPT RHYTHM)
e.g. domperidone

71
Q

Define Ascites

A

Abnormal accumulation of free fluid in the peritoneal cavity

72
Q

What is the most common cause of ascites and how does this cause ascites?

A

Cirrhosis- causes release of NO&raquo_space; peripheral vasodilation&raquo_space; lowering effective blood volume

73
Q

Name two states that contribute to oedema…

A

hypoalbuminaemia and portal hypertension

74
Q

What is the pathophysiology of ascites?

A

Cirrhosis&raquo_space; lower blood vol&raquo_space; sympathetic NS and RAAS activated&raquo_space; renal salt and water retention

There is an imbalance of P. between the circulation (high P.) and the abdominal cavity (low P.). The increase in portal BP and decrease in albumin&raquo_space; forms P. gradient&raquo_space; ascites

75
Q

Name some other causes of ascites?

A

Pancreatitis (indicated by amylase in paracentesis), congestive HF and kidney failure

76
Q

What are the clinical features of ascites?

A
  • fullness in flanks
  • shifting dullness
  • peripheral oedema and pleural effusion may be present
    NO TYMPANIC PERCUSSION
77
Q

What investigations would you do in ascites?

A
  1. Physical examination- perfectly round ball, umbilical hernia, prominent veins
  2. Paracentesis then
  3. Check albumin, amylase and neutrophil count
  4. gram stain and culture for bacteria and acid fast bacilli
  5. Cytology for malignant cells
78
Q

What is the management of ascites?

A
  1. treat the underlying cause
  2. decrease salt intake (diet and drugs): diuretic = begin with sodium restriction&raquo_space; spironolactone&raquo_space; add furosemide (aim is 0.5kg of body mass per day)
  3. paracentesis to drain fluid
79
Q

What complications are associated with ascites?

A

SBP- occurs in 8% of cirrhotic patients with ascites (E-coli)

80
Q

What is the difference between transudate and exudate?

A

Transudate is fluid pushed through the capillary due to high pressure within the capillary. Exudate is fluid that leaks around the cells of the capillaries caused by inflammation.

Transudate is due to increased hydrostatic pressure
Exudate is due to increased permeability

81
Q

What are the causes of exudate?

A

cancer, sepsis, TB. nephrotic syndrome

82
Q

What are the causes of transudate?

A

cirrhosis, cardiac failure, Budd-Chiari syndrome

83
Q

What does albumin in ascites fluid suggest?

A

ascitic albumin less than 11g/L suggests exudate

84
Q

What does the neutrophil count suggest in ascites?

A

neutrophil count >250cells/mm3 suggests SBP spontaneous bacterial peritonitis

85
Q

Why would you look at amylase in paracentesis of ascites?

A

Elevated amylase levels would suggests pancreatic ascites or stone in the common bile duct at Sphincter of Oddi

86
Q

If a patient with ascites gets a SBP what is the treatment?

A

antibiotic therapy: IV cefuroxime

Prophylaxis with norfloxacin from then onwards and referral to liver transplant centre

87
Q

After paracentesis in ascites what would you immediately give to the patient?

A

ALBUMIN as hypoalbuminaemia&raquo_space; P. gradient&raquo_space; ascites

88
Q

When giving diuretics in ascites what is a severe complication?

A

can cause hypokalaemia&raquo_space; encephalopathy

89
Q

H-pylori is associated with an increased risk of which cancer?

A

Gastric cancer

90
Q

Name some non-diarrhoeal causes of GI infection…

A

H-pylori (gastritis), acute cholecystokinin, peritonitis, typhoid, amoebic liver abscess

91
Q

Describe h-pylori

A

Gram -ve, urease producing spiral shaped bacterium, found in gastric antrum and areas of gastric metaplasia in duodenum

92
Q

Describe the epidemiology of h-pylori

A
  • acquired in childhood
  • persists for life unless treated
  • incidence increases with age
  • more common in dev countries (lower socio economic status)
93
Q

How is h-pylori transmitted?

A

Oral-oral or oral-faecal route

94
Q

Give two methods of diagnosing h-pylori

A
  1. Non-invasive = stool antigen testing or urea breath test

2. Invasive = Antrum biopsy during endoscopy (CLO test)

95
Q

Which groups of people are at risk of diarrhoea?

A
  • poor personal hygiene
  • children at nursery/preschool
  • preparing or serving uncooked food
  • HCWs or social care staff working with vulnerable people
96
Q

When is diarrhoea classed as acute?

A

Less than 14 days

97
Q

Define travellers diarrhoea

A

3 or more unformed stools per day AND at least one from: a do plain, nausea, dysentery, cramps

98
Q

When does travellers diarrhoea occur?

A

Within 3 days of arrival in a new country

99
Q

What are the causes of travellers diarrhoea?

A 
ETEC (50-60%)
SE Asia = mainly camplyobacteria
Norovirus
Giardia
Salmonella and Shigella
100
Q

What type of diarrhoea is clostridium difficile?

A

Antibiotic associated

101
Q

Give some causes of dysphagia?

A
  • oral, pharyngeal or oesophageal
  • mechanical or motility related
    e.g. achalasia, systemic sclerosis = motility
    strictures, extrinsic pressure (lung cancer), pharyngeal pouch = mechanical
102
Q

What is achalasia?

A

failure of relaxation of the LOS (due to degeneration of myenteric plexus)&raquo_space; impaired oesophageal emptying

103
Q

What are the symptoms of achalasia?

A

Dysphagia (liquids and solids)&raquo_space; decrease weight
Retrosternal chest pain
Regurgitation

104
Q

Give some investigations for achalasia and what they would show?

A
  1. Barium swallow (marshmallow test)&raquo_space; dilated oesophagus and beak deformity
  2. oesophageal manometry (CONFIRMS DIAGNOSIS)
  3. CXR to check fluid levels in oesophagus
105
Q

What is oesophageal manometry?

A

a test used to measure the function of the lower oesophageal sphincter and the muscles of the oesophagus

106
Q

What is the management of achalasia?

A
  1. endoscopic balloon dilation followed by PPIs
  2. CCB’s (nifedipine) or nitrates to relax LOS
  3. botulinum toxin injections every few months (used in elderly/frail as it is non-invasive)
107
Q

What are the complications of achalasia?

A

Can cause oesophageal cancer (due to food accumulation in oesophagus&raquo_space; inflammation)

108
Q

What is systemic sclerosis?

A

multi system disease with uncontrolled and irreversible proliferation of connective tissue with collagen deposition and thickening of vascular walls

109
Q

What type of systemic sclerosis is seen in GI?

A

Diffuse systemic sclerosis

110
Q

What is the pathophysiology of diffuse systemic sclerosis?

A

smooth muscle layer is replaced with fibrous tissue&raquo_space; decrease in LOS pressure&raquo_space; reflux

111
Q

What are the complications on systemic sclerosis?

A 
CREST
C- calcinassi of subcutaneous tissue
R- raynauds
E- oesophageal and gut motility
S- sclerodactlyly (swollen, tight digits)
T- telangiectasia (spider veins)
112
Q

Which antibodies are seen in systemic sclerosis?

A

Anti Po in 40%

Anti RNA polymerase in 20%

113
Q

What sign would you see in systemic sclerosis?

A

microstomia- small, narrow mouth which is cosmetically and functionally disabling

114
Q

What is the management of systemic sclerosis?

A

NO CURE

  • immunosuppressive routines (IV cyclophosphamide) if organ involvement
    2) regular ACEi / ARBs to decrease risk of renal crisis
115
Q

What needs to be monitored in those with systemic sclerosis?

A

monitor BP and renal function AND annual echocardiogram and spirometry

116
Q

What are the symptoms of a diffuse oesophageal spasm and what would be seen on a barium swallow?

A

intermitted dysphagia +- chest pain

abnormal contractions and corkscrew appearance

117
Q

What is the main cause of appendicitis?

A

Faecolith (poo rock)

118
Q

Give some other causes of appendicitis?

A

undigested seeds, pinworm, lymphoid hyperplasia?

119
Q

Which two groups of people is appendicitis rare in?

A

Very young and very old

120
Q

Describe the pathophysiology of appendicitis…

A

obstruction in lumen of appendix&raquo_space; increased P. of annex (due to buildup of fluid and mucus)&raquo_space; pushes on visceral nerves nearby (abdominal pain)&raquo_space; gut flora multiply&raquo_space; immune response&raquo_space; pus accumulation in appendix

121
Q

What is the clinical presentation of appendicitis?

A

central abdo pain&raquo_space; becomes localised to RID
pain is worse on movement
N & V, weight loss (anorexia), diarrhoea, pyrexia
Rebound tenderness and guarding over RIF

122
Q

What investigations would you do in appendicitis?

A

Inflammatory markers- raised CRP

FBC = neutrophil leucocytosis (raised neutrophils in blood)

123
Q

What is the management of appendicitis?

A

Appendectomy (either open surgery or laparoscopically) then antibiotics

124
Q

What are the complications associated with appendicitis?

A

If appendix ruptures&raquo_space; bacteria escape into peritoneum&raquo_space; peritonitis

125
Q

Give a D/D of appendicitis in females of child bearing age?

A

Ectopic pregnancy (abdominal pain in hypogastric), child bearing age, hypotensive and tachycardia)

126
Q

When would a laparoscopy be performed instead of open surgery?

A

In women or those people that are obese

127
Q

What gut organisms are most responsible for appendicitis?

A

E-coli and bacteroides fragilis

128
Q

Describe the pathophysiology of acute pancreatitis

A

acute inflammation of pancreas due to enzyme mediated auto digestion. This damage is reversible.

129
Q

How can acute pancreatitis be classified?

A

Oedematous (75%)
Severe/necrotising (25%)
Haemorrhagic (5%)

130
Q

Give the causes of acute pancreatitis…

A 
GET SMASHED
G = gallstones
E = ethanol
T = trauma
S = steroids
M = mumps
A = autoimmune (PAN)
S = scorpion venom
H = hyperlipidaemia, hypercalcaemia, hypothermia
E = ERCP and emboli
D = drugs (azothiaprine, diuretics, NSAIDs)
Others = pregnancy,
131
Q

What are the symptoms of acute pancreatitis?

A 
severe epigastric pain radiates into back
pain relieved by sitting forward
pain can be gradual or sudden onset
vomiting
nausea and anorexia
132
Q

What are the signs of acute pancreatitis?

A 
fever, dehydration, hypotension, tachcardia, SHOCK, jaundice
abdominal guarding 
rigidity on examination
Grey Turners sign
Cullens sign
133
Q

What is ‘Grey Turner’s’ sign?

A

bruising of flanks

134
Q

What is ‘Cullen’s’ sign?

A

bruising of the periumbilical region

135
Q

What is the medical term for bruising?

A

ecchymosis

136
Q

What is the diagnostic criteria for acute pancreatitis?

A

2 out of 3 of:

  • severe epigastric pain radiating to back
  • serum amylase >1000 or greater than 3x upper level
  • abdominal CT pathology e.g. loss of fat planes/pancreatic oedema and swelling
137
Q

What scoring system is used in acute pancreatitis to predict the severity of the disease?

A 
Modified Glasgow criteria- score > 3 indicates need for supportive ITU treatment
P: PaCO2 <8kPa
A: Age >55yrs
N: neutrophilia WCC> 15x10^9/L
C: calcium <2mmol/L
R: renal function = urea >16mmol/L
E: enzymes = LDH >600 &amp; AST >200
A: albumin <32g/L (serum)
S: sugar (blood glucose >10mmol/L)
138
Q

What is the Ranson criteria?

A

Used to detect pancreatitis severity
>=3 = severe
*can only be fully applied after 48hrs

139
Q

How is acute pancreatitis managed?

A

SEVERITY ASSESSMENT = ESSENTIAL
1. Analgesia (pethidine): avoid morphine as increases P. of Spincter of Oddi)
2. ABCDE approach to reuses- inc. catheterisation and nutrition (Nil by mouth likely to need NG tube) and IV fluids
3. drain collections&raquo_space; culture to find antibiotic
4. CT or MRI to confirm diagnosis
5. ERCP within 48hr if gallstone pancreatitis
ANTIBIOTICS: metronidazole or cefuroxime

140
Q

What are the short term complications of pancreatitis?

A

acute complications = hyperglycaemia, hypocalcaemia, renal failure and shock

141
Q

What are the long term complications of pancreatitis?

A

MODS- multiple organ dysfunction syndrome- consequence of AP and leads to loss of homeostatic mechanisms
abscesses
bleeding due to elastase eroding major vessel e.g. splenic artery
thrombosis&raquo_space; bowel necrosis

142
Q

What is SIRS? and how is it diagnosed?

A 
Systemic inflammatory response syndrome- pro inflammatory state with no known source of infection
Diagnosis = 2 or more of the following:
1. tachycardia >90bpm
2. tachypnoea >20 breaths per min
3. pyrexia >38 or hypothermia <36
4. WCC > 12x10^9
143
Q

How can the progress of treatment in acute pancreatitis be monitored?

A

repeat CT

144
Q

What is the epidemiology of chronic pancreatitis?

A

More common in men 4:1

145
Q

What is the pathophysiology of chronic pancreatitis?

A

Unknown- suggested that obstruction or reduction in bicarb excretion leads to activation of pancreatic enzymes&raquo_space; tissue necrosis and fibrosis

146
Q

What are the causes of chronic pancreatitis?

A

most common cause in developed countries = alcohol

others = tropical chronic pancreatitis, hereditary, autoimmune, and CF

147
Q

What are the clinical features of chronic pancreatitis?

A

epigastric abdo pain (radiates to back)
severe weight loss due to anorexia
diabetes and steatorrhoea may develop due to endocrine (insulin) and exocrine (lipase) insufficiency
Occasionally jaundice is presenting symptoms

148
Q

What is the D/D in chronic pancreatitis?

A

Pancreatic cancer- also presents with pain and weight loss and may develop on the backdrop of chronic pancreatitis

149
Q

What tests are diagnostic in chronic pancreatitis?

A

diagnosis made by imaging (demonstrations`te structural changes in the gland) and metabolic studies (demonstrates functional abnormalities)

150
Q

What investigations are used in chronic pancreatitis?

A

Radiology:

  • plain abdo x-ray will show pancreatic calcification
  • US and CT may show calcifications, ductal dilatation, an outline of gland and fluid collections

Functional assessment- insensitive in early stages

  • faecal elastase from stool sample is reduced
  • raised blood sugar indicates DM
151
Q

What is the treatment for chronic pancreatitis?

A

1) stop taking alcohol
2) opiates for pain control (risk of addiction)
3) pancreatic enzyme supplements
4) treat diabetes

If severe disease and intractable pain = surgical resection + drainage of pancreatic duct (pancreaticojejunostomy)

152
Q

What is the difference in presentation between endocrine and exocrine dysfunction in chronic pancreatitis?

A

Exocrine = malabsorption with weight loss, diarrhoea, steatorrhoea (pale, loose, offensive stools) and protein def

Endocrine = diabetes mellitus

Phase 2a (7 decks)

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