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Gasterointestinal Flashcards

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1
Q

Causes of massive splenomegaly

A 
CML
Myelofibrosis
Lymphoma (marginal zone)
Hairy cell leukaemia
Gaucher
Thalassaemia
Malaria
Kala Azar
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2
Q

What is Gaucher disease?

A

A genetic disease in which fatty substances (sphingolipids) accumulate in cells. Gaucher’s disease is the most common of the lysosomal storage diseases.

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3
Q

Infectious causes of splenomegaly

A

Viral - EBV, CMV, HIV
Bacterial - TB, brucellosis, IE
Paracytic - Malaria, bilharzia (schistosoma), leishmania
* abscess

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4
Q

Infiltrative causes of splenomegaly

A

Malignancy - Myeloproliferative and lymphoproliferative disorders
Amyloidosis
Storage diseases - Gaucher’s

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5
Q

Non-infectious inflammatory causes of splenomegaly

A

RA
SLE
Sarcoidosis

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6
Q

Definition of heartburn

A

A retrosternal burning pain that can spread to the neck or chest. Worst when lying down or bending. Often associated with certain foods. May be an epigastric component

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7
Q

Definition of regurgitation

A

The effortless reflux of oesophageal contents into the mouth and pharynx

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8
Q

Definition of GORD

A

A condition which develops when the reflux of stomach contents causes symptoms and/or complications
Two most common symptoms are heartburn and regurgeitation

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9
Q

What are the extra-oesophageal symptoms of GORD

A

Asthma

Chronic cough or laryngitis

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10
Q

GORD vs. IHD

A 
Reflux pain: burning
1. worse on bending, lying down, hot drinks or alcohol
2. Seldom radiates to the arms
3. Relieved by antacids
4. No association with exertion
Ischaemic pain: gripping or crushing
1. Radiates to neck or left arm
2. Worse with exercise; accompanied by dyspnoea
3. Palpitations and sweating
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11
Q

Pathophysiology of GORD

A

Occurs when anti-reflux mechanisms fail, allowing acidic gastric contents to make contact with the lower oesophageal mucosa
Most important cause: when sphincter relaxes transiently independent of a swallow –> Transient Lower Oesophageal Sphincter Relaxations (TLESR)

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12
Q

Anti-reflux mechanisms

A

Lower oesophageal sphincter: most NB. Smooth muscle contracts at rest, relaxes transiently to allow passage of food and wind; distal end of oesophagus; small amounts of reflux are normal
Intra-abdominal segment of oesophagus acts as a valve
Crural diaphragm at the level of the LOS acts like a pinchcock
Oesophageal acid clearance
Saliva neutralises refluxed acid

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13
Q

Risk factors for GORD

A 
Pregnancy or obesity
Fat, chocolate, coffee or alcohol ingestion
Large meals
Cigarette smoking
Drugs: CCBs; nitrates
Systemic sclerosis (--. oes dysmotility)
Reduced saliva production (xerostomia)
After treatment for achalasia
Hiatus hernia
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14
Q

What is a sliding hiatus hernia and how does it disrupt anti-reflux mechanisms

A

= part of the stomach slides through the hiatus to lie above diaphragm
Disrupts:
1. loss of intra-abdominal segment of oes
2. loss of crural diaphragm at level of LOS
3. oesophageal clearance delayed in the rpesence of a hiatal sac

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15
Q

How do you diagnosis GORD

A

Presumptive diagnosis established if there are typical symptoms of heartburn and regurgitation
Upper endoscopy not required if normal symtpoms;
Endoscopy done if alarm signs: dysphagia; LOW; GIT bleeding

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16
Q

Management of GORD

A

Lose weight
Cut out fatty food, chocolate, peppermints, alcohol, coffee
Raise head of bed
Antacids
If severe symptoms: H2-receptor antagonists and PPIs usually required
If no response, test further - endoscopy; pH manometry

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17
Q

Complications of GORD

A

Peptic Stricture

Barrett’s oesophagus

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18
Q

What is Barrett’s oesophagus

A

Part of normal oesophageal squamous epithelium is replaced by metaplastic columnar mucosa to form a segment of columnar-lined oesophagus.
‘intestinal metaplasia’
Premalignant - predisposes to adenocarcinoma

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19
Q

Which GORD patients should not have surgical therapy

A

Those with oesophageal dysmotility, who do not respond to PPIs or who ahve functional disease

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20
Q

Definition of dyspepsia

A

Epigastric pain or discomfort, often burning (predominant symptom- helps distinguish from GORD)
Other symptoms of early satiety, bloating or heartburn

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21
Q

Causes of dyspepsia

A 
Functional
Gastric-oesophageal malignancy
Peptic ulcer disease
Gastroparesis
Gastritis
Biliary colic
Pancreatic pain
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22
Q

Approach to dyspepsia

A 
History: 
- alarm features
- NSAID use
- family hx
Examination:
- abdo mass
- nodes
- pallor
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23
Q

Alarm features of dyspepsia

A 
>45 years of age (new onset)
Haematemesis, rectal bleeding or malaena
Significant LOW and anorexia
Persistent vomiting
Dysphagia or odynophagia
Family history of upper GIT cancer
Previous gastric surgery or peptic ulcer
Previous gastric malignancy
Anaemia, abdo mass, lymphadenopathy
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24
Q

Empiric management for dyspepsia

A

Antacids
H2 receptor agonists
PPI
Test and treat for H Pylori

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25
Which dyspeptic patients do you refer for a scope
Alarm features (refer ASAP) Age >45 (refer ASAP) No response after 4-5/52 rx Recurrent
26
Duodenal vs. gastric ulcers
Duodenal: usually at duodenal bulb; + pain with fasting; not associated with cancer Gastric: usually at angulus of the lesser curve; + pain with eating; 1-3% gastric CA presents as ulcers
27
Presentation of PUD
Epigastric pain LOA and LOW Nausea and vomiting Haematemesis and malaena
28
Causes of PUD
Helicobacter pylori | NSAIDs and salicylates
29
Differential diagnosis of upper GIT ulceration
``` PUD Infections IBD- Crohn's Vasculitis Drugs: cocaine, bisphosphonates Chemo-radiation Malignancy ```
30
What 4 GIT diseases is H. pylori a cofactor for
Antral gastritis Duodenal or gastric ulcers Gastric CA Gastric mucosa-associated lymphoid tissue (MALT) lymphoma
31
Which patients are at risk for complicated PUD with NSAIDS
``` Advanced age (>65 years) Previous PUD High dose NSAIDs >1 NSAID use Concurrent steroid use Concurrent warfarin Other medical disorders Anticoagulants ```
32
Complications of PUD and rx
Gastric outlet obstruction - endoscopic dilatation or stenting Bleeding - endoscopic control or surgery Perforation - omental patch
33
H. pylori eradication therapy
At least 2 abx with 2/52 PPI Abx: metronidazole, clarithromycin, amoxicillin, tetracycline and bismuth Successful eradication should ideally be confirmed by non-invasive tests or follow-up endoscopy
34
Non-invasive H pylori tests
C14/13 urea breath test | Stool antigen
35
What is the rapid urease test
Antral biopsy performed at g-scope - | H pylori produces urease --> breaks down ammonia --> increase pH --> colour change
36
Relationship between NSAIDs and PUD
30% chronic NSAID users will get PUD and 1-2% will bleed/perforate NSAID ulcers may be assymptomatic Different NSAID: different risk Low-dose aspirin = definite risk for GI complications
37
Management of PUD
``` Stop NSAIDs if possibl Long term PPI prophylaxis after ulcer heals to prevent reccurrence (if NSAID/aspirin cannot be stopped) Stop smoking and alcohol Start acid suppression: PPIs = best Rx H pylori ```
38
What are the criteria to make the diagnosis of functional constipation
Rome III Diagnostic Criteria - symptoms >3/12, onset >6/12 prior to dx Symptoms (>2): - straining - lumpy/hard stools - sensation of incomplete evacuation - sensation of anorectal obstruction/ blockage - manual maneuvers to facilitate defecation -
39
Criteria for IBS-C
= recurrent abdo pain/ discomfort >3/12 days/month for the last 3/12 Symptoms (>2): - improvement with defecation - onset associated with change in stool frequency - onset associated with change in stool form Subtyped as epr predominant stool pattern- IBS-C = hard/lumpy stools >25%, loose/watery
40
Types of functional constipation
Normal transit Slow transit Dyssynergic defecation IBS-C (MC)
41
Causes of secondary constipation with example of each
Organic (colorectal CA) Endocrine/ metabolic (DM/ hypothyroid) Neurological (spinal cord injury, Parkinsons) Myogenic (scleroderma, amyloid) Anorectal (anal fissure/ stricture) Drugs (opiates, TCAs, anti-hypertensive agents) Diet (low fibre; dehydration; inactive lifestyle)
42
What is the bristol stool chart and how is it relevant in diagnosis of constipation
Used in clinical trials Correlates with symptoms of straining and difficult evacuation Correlates with colonic transit Majority of constipated patients have stool types 1-3
43
Alarm features of constipation
``` Haematochezia FHx colonCA FHx of IBD Anaemia Positive faecal occult blood test Unexplained LOW New/ recent onset constipation ```
44
Mechanisms of constipation in elderly
Changes in colonic motility and physiology predispose patient to constipation. Changes include: - Reduced number of mystenteric plexus - Increased collagen deposition - compliance and dysmotility - Decrease inhibitory input - coordination
45
Likely diagnosis(/es) if constipated + associated significant LOW + PR bleeding
Organic pathology | Cancer
46
Likely cause of constipation if patient also has worsening diabetic control
DM Autonomic dysfunction Renal dysfunction
47
Likely cause- Patient with constipation + moans and groans
Hypercalcaemia Myeloma Hyperparathyroid CA
48
Likely cause- Patient constipated + history of falls + difficulty walking
Spinal cord- disc / CA
49
Likely cause- Patient constipated + increasing confusion + tremor
Parkinsonism
50
Likely cause - Patient constipated + has uncontrolled HPT
CCB use
51
Types of laxatives
``` Bulk forming Stool softening Osmotic Stimulant Suppositories and enemas ```
52
Manifestations of GIT bleeding
``` GIT specific: -Haematemesis -Melaena -Haematochezia General: - hypotension - anaemia - can be asymmptomatic ```
53
Difference between haematochezia and melena
Transit time: oxidation of iron in Hb takes +/- 14 hours : Transit time haematochezia >14 hours --> melena * site does not define the difference: - smaller bleed typically longer transit so can be lower (reduced peristalsis) - large upper GI bleed --> increased motility, slower transit and presents as haematochezia
54
Characteristics of melena
Black Tarry Foul-smelling
55
4 categories of GI bleeds
Acute Upper Chronic Upper Acute Lower Chronic Lower
56
What divides the upper from lower GIT
Ligament of Treitz = cross-over between the duodenum and jejunum
57
Sites of GI bleeding
``` Oesophagitis Varices Peptic ulcer Mallory-Weiss tear Vascular malformations CA oesophagus/ stomach Gastric erosions Aorto-duodenal fistula ```
58
Division of causes of acute upper GI bleeds
Variceal or Non-variceal
59
Indicators of severity of acute upper GI bleed
Volume: generally overestimated by px, unreliable Frequency Melena or haematochezia: volume, frequency Nature: -fresh blood: large bleed, variceal haemorrhage, MW tear - Coffee-ground: limited bleeding
60
NB questions on history for a patient with an acute upper GI bleed
Previous GI bleeding/ g-scope Accompanying symptoms: dysphagia/odynophagia, reflux symptoms, epigastric pain, LOW, change in bowel habits Med use: NSAIDs, warfarin,/ aspirin/ clopedogrel, PPIs/ prev eradication therapy, corticosteroids, COC Social history: ETOH, smoking Risk factors for CLD: alcohol abuse, HBV/ HCV, FHx liver disease Previous surgery: aortic, abdominal (esp. gastric)
61
Components of risk stratification in patients with acute upper GI bleed
1. Identify high risk patients: - Presentation: majoy bleed with decompensated shock; low Hb - Pathology: varices, penetrating peptic ulcer - Co-morbid factors: more susceptible to hypoxaemia (IHD, lung disease); more susceptible to fluid overload (CKD, cardiac failure), bleeding more difficult to control (coagulopathies, thrombocytopaenia), predisposed to aspiration (encephalopathy, dementia) 2. Early referral to specialised unit 3. Appropriate in-hospital monitoring 4. Early discharge
62
System used for risk stratification in upper GI bleed
Modified Rockall Scoring System | Max score prior to endoscopy and following endoscopy give risk of death %
63
If doing a g-scope for upper GI bleed, when and where do you scope and when do you rescope
Timing: - Emergency: unstable px, continued bleeding - Urgent: varices suspected, high risk patient, elderly, shocked - Elective: 12-24 hours "next morning" Where: endoscopy unit if stable; theatre if unstable Rescope if first scope unsatisfactory
64
Classification system for peptic ulcer bleeding
Forrest classification Classifies into low vs. high risk (rebleeding and mortality risk)- serves as a guide for therapeutic interventions Acute haemorrhage: Forrest Ia (spurting) or Forrest Ib (oozing) Recent h'ge: F IIa (visible vessel), IIb (adherent clot), F IIc (flat pigmented haematin on ulcer base) No active bleeding: F III (no signs of recent h'ge; fibrin-covered clean ulcer base)
65
Endoscopic management of upper GI bleeds - indication and methods
Indication: >/= Forrest II b Dual therapy recommended: 1. Adrenaline injection: safe, effective, inexpensive, no maintenance, portable, available, easy; vasoconstriction and volume compression effect 2. Thermal therapy: direct thermal coagulation through direct application of heater probe to BV 3. Clipping devices: detachable clip onto BV
66
Classification system used for risk stratification in portal hypertension
Child-Pugh | Bili, Albumin, INR, Ascites, Encephalopathy
67
Control of acute variceal bleed
1. Pharmacotherapy 2. Correct coagulopathies 3. Endoscopic therapy - band ligation, injection sclerotherapy, combo therapy 4. Sengstaken tube 5. Shunt procedure
68
Different colour PR bleeds
Black - upper GIT bleed or mild more proximal lower GIT bleed Dark red: larger upper GIT or more proximal lower GIT bleed Bright red: distal or anal source of bleeding
69
Nature of PR bleeding
Melena Fresh blood Mixed with stools Not mixed with stools
70
Accompanying symptoms of PR bleeding
``` Abdo pain (location/ nature) LOW Fever Hx constipation/ diarrhoea Change in bowel habits Tenesmus Pain on passing stools ```
71
Different types of endoscopy for PR bleeding
Sigmoidoscopy Colonoscopy Gastroscopy
72
Causes of PR bleeds
``` Angiodysplasia Ischaemic colitis Colitis (infections, IBS) Polyps Carcinoma Diverticula Haemorrhoids ```
73
Definitions of obscure, overt and occult bleeding
Obscure: bleeding that persists or recurs without an obvious aetiology after upper endoscopy, colonscopy and radiologic evaluation of the small bowel. Subdivided into overt and occult Overt - visible blood loss Occult: positive FOBT and/or IDA but no evidence of visible blood loss
74
Red flags in acute diarrhoea
``` Blood in stool Recent hospitalisation/ abx Profuse with dehydration Abdominal mass/ tenderness LOW Fever ```
75
Causes of acute diarrhoea
Bacteria (campylobacter, salmonella, shigella, e. coli, c diff0 Protozoa/ parasites (cryptosporidia, giardia, e histolytica, cyclospora) Viruses (novavirus, rotavirus) Food allergies Food poisoning Medications
76
Causes of chronic diarrhoea
Infections (TB, protozoa, CMV, HSV) Malabsorption (SBO, coeliac disease, short bowel syndrome) Maldigestion (pancreatic exocrine insufficiency0 IBD Neoplasia Endocrine disease Laxative abuse

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