Gastroenterology (Bleeds, Constipation, Diarrhoea and Dysphagia) Flashcards

1
Q

causes of upper GI bleeds: Variceal vs Non-variceal

A

Variceal
- oseophageal varices secondary to portal hypertension in liver cirrhosis

Non-variceal
- peptic ulcer (most common)
- Mallory weis tear
- Stomach cancers

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2
Q

presentation of acute upper GI bleed

A
  • Haematemesis – vomiting blood
  • This can be bright red or described as ‘coffee grounds’
  • Melaena – describes the passage of digested blood as black, tarry stools
  • Nausea and vomiting – blood in the GI tract is pro-emetic
  • Increased urea levels:
    ->Helps distinguish lower GI and upper GI bleeds as the digestion of blood increases urea
  • Signs and symptoms of associated diagnoses (e.g. stigmata of liver disease)
  • Signs of decompensation – tachycardia or hypotension
  • Heart rate is a better measure as blood pressure initially can remain normal
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3
Q

risk assessment scores for upper GI bleed

A

The Blatchford score – done at first assessment

The full Rockall score – done after endoscopy

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4
Q

the blatchford score

A

Done at first assessment

It estimates the risk of the patient having an upper GI bleed and therefore if they can be management as an outpatient.

  • A score above 0 indicates a high risk for an upper GI bleed.
  • The NICE guidelines (updated 2016) suggest considering early discharge in patients with a score of 0.

The easiest way to calculate the score is using an online calculator. It takes into account:

  • Haemoglobin (falls in upper GI bleeding)
  • Urea (rises in upper GI bleeding)
  • Systolic blood pressure
  • Heart rate
  • Presence of melaena (black, tarry stools)
  • Syncope (loss of consciousness)
  • Liver disease
  • Heart failure
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5
Q

Rockall score

A

Done after endoscopy

Estimates the risk of rebleeding and mortality.

It takes into account:

  • Age
  • Features of shock (e.g., tachycardia or hypotension)
  • Co-morbidities
  • Cause of bleeding (e.g., Mallory-Weiss tear or malignancy)
  • Endoscopic findings of recent bleeding (e.g., clots and visible bleeding vessels)
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6
Q

emergency management of upper GI bleed

A

The initial management can be remembered with the ABATED mnemonic:

  • A – ABCDE approach to immediate resuscitation
  • B – Bloods
  • A – Access (ideally 2 x large bore cannula)
  • T – Transfusions are required
  • E – Endoscopy (within 24 hours)
  • D – Drugs (stop anticoagulants and NSAIDs)
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7
Q

blood tests for Upper GI bleed

A
  • Full blood count – may identify anaemia or thrombocytopenia
  • Crossmatching – in case blood products are necessary
  • Coagulation profile – to identify coagulopathy
  • Liver function tests – to identify underlying liver disease
  • Urea and electrolytes – urea is elevated in UGIB
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8
Q

blood transfusion for upper GI bleed

A
  • Blood, platelets and fresh frozen plasma are given to patients with massive bleeding
  • Transfusing more blood than necessary can be harmful
  • Platelets are given in active bleeding plus thrombocytopenia (platelet count less than 50)
  • Prothrombin complex concentrate can be given to patients taking warfarin that are actively bleeding
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9
Q

management of Upper GI bleed caused by Variceal bleeding

A

Before OGD

  • Terlipressin
  • Broad spec antibiotics

During endoscopy
- Variceal band ligation

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10
Q

management of Upper GI bleed caused by non- variceal bleeding

A

do not give PPI before endoscopy
OGD
- can be treated with adrenaline or clips or thermal coagulation

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11
Q

Lower gastrointestinal bleeding (LGIB)

A

describes bleeding occurring distal to the ileocaecal valve (i.e. the colon, rectum, and anus). It is common, and most cases are due to benign causes, however, there are many other possible causes, including malignancy.

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12
Q

presentation of lower GI bleed

A
  • bright or dark red blood
  • blood generally accelerates intestinal transit time, meaning it is expelled sooner and before enzymatic digestion
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13
Q

investigations for lower GI bleed

A

Full blood count (FBC):

  • May show anaemia
  • Increased white cell counts suggest infection
  • May show thrombocytopenia which can predispose to bleeding

Clotting studies:

  • May show clotting abnormalities such as increased INR, PT, or APTT

Group and save:

  • Determines patient blood group and screens for atypical antibodies
  • A crossmatch may be considered which is where red cell products are provided to the patient

Iron studies:

  • May show iron-deficiency anaemia

Urea and electrolytes:

  • May show elevated urea suggesting a UGIB

Liver function tests:

  • May be deranged suggesting liver cirrhosis
  • Low albumin may occur due to liver cirrhosis or protein-losing enteropathy

C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR):

  • May be elevated in inflammatory bowel disease

Faecal calprotectin:

  • Considered if inflammatory bowel disease is suspected

Stool culture tests:

  • If infective causes are suspected

Testing for sexually-transmitted infections:

  • May be considered
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14
Q

Lower GI bleeds: Haemodynamically unstable patients

A

Patients with haemodynamic instability (e.g. those with hypotension) should first be resuscitated. Investigations may then include:

Urgent CT angiogram (CTA) – before endoscopy

  • This can localise the bleeding site and therapies to stop bleeding (e.g. embolisation) can be performed to stabilise the patient

Upper GI endoscopy:

  • May be considered if the CTA cannot localise the bleed site

Emergency laparotomy:

  • If a CTA and endoscopy fail to locate the bleeding site
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15
Q

Haemodynamically stable patients: Lower GI bleed

A

Blood transfusions may initially be considered. Following this, investigations may involve:

Colonoscopy:
* May identify masses and allows for therapeutic intervention

Upper GI endoscopy:
* If colonoscopy does not identify any causes

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16
Q

differentials for lower GI bleed

A
  • Haemorrhoids
  • Anal fissures
  • Diverticular disease
  • Crohns disease
  • UC
  • Lower GI cancer
  • Infectious gastroeteritis
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17
Q

constipation definitions

A

Constipation describes problems with defecation due to hard stools, difficulty passing them, or the sensation of incomplete emptying or anorectal blockage. Chronic constipation is where these symptoms are present for at least 3 months.

Faecal impaction (or loading) describes the retention of faeces to the point where spontaneous passage is unlikely.

Overflow faecal incontinence (also known as encopresis or bypass soiling) describes leakage of liquid stool around impacted faeces.

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18
Q

Constipation can be divided into:

A
  • Primary (or idiopathic) – such as irritable bowel syndrome-C (IBS-C)
  • Secondary (or organic) – constipation caused by an underlying cause such as a drug or medical condition
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19
Q

secondary causes of constipation

A

Drugs
- Opioids
- Anticholinergics e.g. tricyclic antidepressants
- CCBs
- Antipsychotics

Structural disorders
- Anal fissures
- HAemorrhoids
- Colonic stircutre
- IBD
- Obstruction
- Mass
- Diverticulosis

Endocrine
- Hypothyroidism
- Hypercalcaemia and hyperparathryoidism
- DM
- Hypokalameia

Neuro
- Stroke
- MS
- Parkinsons
- Spinal cord injury
- Brain tumour

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20
Q

presentation of constipation

A
  • Bowel movements <3 times a week may be considered constipation
  • Constipation is generally considered when stools are passed less frequently than what is normal for the patient
  • There may be additional symptoms such as abdominal pain, discomfort, or bloating
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21
Q

Elderly people and constipation

A

Elderly patients may have non-specific symptoms:

  • Confusion or delirium
  • Overflow diarrhoea
  • Nausea, vomiting, or loss of appetite
  • Urinary retention
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22
Q

red flags for constipation

A
  • Age >50 years
  • Weight loss
  • Associated symptoms such as rectal bleeding, tenesmus, or discharge
  • Blood in the stool
  • Recent onset of symptoms
  • Symptoms suggesting obstruction
  • Rectal prolapse
  • Change in stool calibre
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23
Q

Constipation investigations

A

Most patients do not require investigation. Some other tests that may be considered are:

  • Full blood count
  • Urea and electrolytes (U&Es)
  • Serum calcium
  • Thyroid function tests
  • Abdominal x-ray
  • Colonoscopy
  • Barium enema
24
Q

management of constipation

A

First line
- lifestyle - increasing fibre
- keeping active
- keeping hydrated

Second line-
- Bulk forming laxatives e.g. Ispaghula husk (avoid in flatulence, bloating)
- Stimulant laxative - senna (avoid in intestinal obstruction)
- Osmotic laxatives - lactulose and macrogol

25
Q

management of faecal impaction

A
  • If hard stools present: high-dose oral macrogol
  • If soft stools present or ongoing hard stools after a few days of oral macrogol treatment, consider starting or adding an oral stimulant laxative

If inadequate response or too slow, consider:
* Bisacodyl suppository, glycerol alone, or glycerol + bisacodyl
* Mini enema e.g. docusate or sodium citrate

26
Q

complications if constipation

A

Chronic constipation can lead to:

  • Faecal impaction
  • Progressive faecal retention
  • Rectal distention and reduced sensorimotor function
  • Haemorrhoids
  • Anal fissures

Faecal impaction can lead to more serious complications:

  • Faecal incontinence
  • Chronic colon dilatation
  • Bowel obstruction, perforation, or ulceration
  • Obstructive uropathy
  • Rectal bleeding
  • Rectal prolapse
27
Q

diarrhoea

A

‘the passage of 3 or more loose or liquid stools per day (or more frequent passage than is normal for the individual)’.

Diarrhoea can be divided into:

  • Acute diarrhoea – lasting <14 days
  • Persistent diarrhoea – lasting >14 days
  • Chronic diarrhoea – lasting >4 weeks
28
Q

investigating acute diarrhoea

A

Most patients do not require testing, however, stool specimens for culture and sensitivity should be arranged if any of the following apply:

  • Systemically unwell, immunocompromised, needs hospital admission, needs antibiotics
  • Has recently had antibiotics, proton pump inhibitors (PPIs), or been in hospital
  • Blood or pus is present in the stool
  • Diarrhoea occurs after foreign travel
  • Diarrhoea is persistent (2 weeks or more) or the cause is uncertain
  • There is a public health indication (e.g. suspected food poisoning, outbreaks of diarrhoea, contacts with certain organisms such as Clostridioides difficile
29
Q

investigations for chronic diarrhoea

A

The following tests should be arranged for all patients:

  • Full blood count (FBC) – may detect anaemia
  • Liver function tests and albumin (LFTs)
  • Thyroid function tests (TFTs)
  • Urea and electrolytes (U&Es)
  • Vitamin B12 and folate
  • Calcium
  • Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)
  • Coeliac disease screening – immunoglobulin A (IgA), and IgA tissue transglutaminase (tTG) or IgA endomysial antibody (EMA)

Further investigations to consider are:

  • CA-125 testing if ovarian cancer is suspected
  • HIV testing if immunodeficiency is suspected
  • Sending stool samples for microbiological investigation and examination if an infection is suspected
  • Faecal calprotectin if inflammatory bowel disease is suspected
  • This should not be used in patients where cancer needs to be ruled out as it may be elevated in cancer
  • Faecal blood tests – for those that do not meet the referral criteria for suspected cancer
30
Q

Emergency hospital admission for acute diarrhoea

A

Emergency admission should be arranged if any of the following apply:

  • Vomiting and unable to retain oral fluids
  • Clinical features of severe dehydration

Other factors that may increase the need for admission depending on clinical judgement:

  • > 60 years old – due to increased risk of complications
  • Support at home
  • Fever
  • Bloody diarrhoea
  • Abdominal pain and tenderness
  • Co-existing comorbidities and drugs used
31
Q

Clostridioides difficile

A

(C. difficile) is a Gram-positive anaerobic rod spread by bacterial spores found in faeces.
- It is known for causing inflammation of the colon.
- Surfaces may be contaminated with spores and spread via the hands of healthcare workers.

32
Q

risk factors C.diff

A
  • Antibiotic use:
  • Common culprits are clindamycin, cephalosporins, ciprofloxacin and carbapenems
  • Increased age
  • Exposure to an infected individual
  • Use of proton pump inhibitors
  • Inflammatory bowel disease (IBD)
  • Immunosuppression
33
Q

C.diff presentation

A

Patients may be asymptomatic, have mild disease, pseudomembranous colitis, or fulminant colitis. Features generally emerge 5-10 days after antibiotic exposure:

  • Watery diarrhoea
  • Abdominal cramps
  • Fever
34
Q

C.diff investigations

A

Full blood count
- WCC raised in 80%

Stool sample testing
1) C. difficile antigen (specifically glutamate dehydrogenase)
2) A and B toxins (by PCR or enzyme immunoassay)

The antigen test shows whether C. difficile is present but not whether it is producing toxins. The antigen is the initial screening test and is followed up with tests for toxins if C. difficile is identified.

35
Q

management of acute c.diff infection

A

1st-line: oral vancomycin
2nd-line: oral fidaxomicin
3rd-line: oral vancomycin with or without IV metronidazole
Vancomycin is poorly absorbed from the gut, making it good for use in C. difficile as it remains there

36
Q

managemet of acute life threating C.diff

A

1st-line: oral vancomycin + IV metronidazole
Seek urgent specialist advice as surgery may be necessary

37
Q

management of recurrent C.diff

A
  • ≤12 weeks of symptom resolution: oral fidaxomicin
  • ≥12 weeks following symptom resolution: oral vancomycin or fidaxomicin
  • Faecal microbiota transplants may be considered in adults who have had ≥2 episodes
38
Q

gastroparessis

A

delayed gastric emptying secondary to reduced peristalsis of the stoamch without mechanical obstruction

39
Q

causes of gastroparesis

A
  • Idiopathic – most common
  • Diabetes mellitus – due to diabetic neuropathy
  • Post-gastric surgery
  • Following bacterial or viral gastroenteritis
  • Multiple sclerosis
  • Parkinson’s disease
  • Post-stroke
  • Hypothyroidism
  • Connective tissue disorders (e.g. systemic sclerosis, systemic lupus erythematosus etc.)
  • Medications (e.g. opioids, tricyclic antidepressants, and anticholinergics)
40
Q

presentation of gastroparesis

A
  • Early satiety
  • Nausea
  • Vomiting
  • Bloating
  • Upper abdominal pain
  • Erratic blood glucose levels – seen in people with diabetes mellitus
41
Q

investigating gastroparesis

A

Investigations

Serum glucose and/or HbA1c:
* Diabetes mellitus can cause gastroparesis

Urea and electrolytes:
* Electrolyte derangements may cause gastroparesis

Serum amylase and/or lipase:
* To rule out pancreatitis if abdominal pain is significant

Total protein and albumin:
- May be decreased in patients with malnutrition

Abdominal x-ray:
- To rule out causes such as bowel obstruction

Endoscopy:
- May be considered to rule out mechanical causes such as malignancy or pyloric stenosis

Gastric emptying scintigraphy:
- A radioactive isotope is given with food and its progression through the GI tract is monitored

42
Q

management of gastroparesis

A
  • Correcting fluid, electrolyte, and nutritional deficiencies
  • Symptom control – prokinetic agents such as metoclopramide or domperidone
  • Anti-emetics may be considered such as promethazine and prochlorperazine
  • Other options include dietary changes, endoscopic botulinum toxin injection, or surgery
43
Q

New-onset dysphagia is a

A

Red-flag symptom.

Regardless of age, symptoms, and other features, urgent endoscopy is required. Any patient, regardless of age and other features, should be offered an urgent upper gastrointestinal endoscopy to be performed within 2 weeks.

44
Q

presentation of dysphagia

A
  • Regurgitation
  • Choking
  • Coughing
  • Vomiting
    Steadily worsening dysphagia may suggest malignancy.
45
Q

referral for dysphagia

A

Any patient, regardless of age and other features, should be offered an urgent upper gastrointestinal endoscopy to be performed within 2 weeks.

46
Q

key differentials for dysphagia

A
  • Acute pharyngitis
  • Oesophageal cancers
  • GORD
  • Oesophagitis
  • Oesophageal candidiasis
  • Achalasia
  • Globus hystericus
  • Pharyngeal pouch
  • Systemic scelrosis
  • MG
  • Stroke
  • Parkinsons
  • MS
47
Q

Oesophageal cancer

A
  • Dysphagia tends to affect solids more than liquids, however, as the disease progresses, dysphagia may affect both
  • Weight loss may be present and may be severe
  • Risk factors such as smoking, alcohol consumption, and longstanding and untreated GORD may be present
48
Q

Gastro-oesophageal reflux disease (GORD)

A

Patients also report heartburn and acid reflux
No other exam findings are generally seen

49
Q

Oesophageal candidiasis

A
  • Patients report odynophagia
  • There may be a predisposing risk factor (e.g. HIV, immunosuppression, inhaled corticosteroid use)
50
Q

Achalasia

A
  • Dysphagia tends to affect both solids and liquids from the start
  • There may be associated regurgitation and heartburn
  • Patients may have coping mechanisms for dysphagia (e.g. sitting or standing up straight when eating)
51
Q

Globus hystericus

A
  • Dysphagia is generally painless, intermittent, and relieved with swallowing
  • There may be a history of a psychiatric problem (e.g. depression or anxiety)
  • The presence of pain warrants further investigation
52
Q

Pharyngeal pouch

A
  • Generally seen in older patients
  • A neck lump that gurgles on palpation may be seen
  • There may be associated regurgitation and cough
  • Halitosis may be seen
53
Q

Systemic sclerosis

A
  • Other features of CREST syndrome may be seen: Calcinosis, Raynaud’s phenomenon, oEsophageal dysmotility, Sclerodactyly, Telangiectasia
  • Anti-Scl-70 antibodies and/or anti-centromere antibodies may be positive
54
Q

Myasthenia gravis

A
  • Features tend to progressively get worse after exertion or at the end of the day
  • Extraocular muscle weakness may be seen, which can cause diplopia
  • Ptosis and proximal muscle weakness may be seen on examination
55
Q

Parkinson’s disease

A
  • Associated coughing, choking, regurgitation, and drooling may be seen
  • Cardinal (TRAP) symptoms of Parkinson’s disease may be present, such as Tremors, Rigidity, Akinesia or bradykinesia, and/or Postural instability
56
Q

Multiple sclerosis

A
  • Associated coughing, choking, regurgitation, and drooling may be seen
  • Associated sensorimotor deficits may be seen, including vision loss due to optic neuritis, and spasticity
  • Urinary incontinence or retention may be seen
57
Q
A