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Gastrointestinal Block > The Breadth of GI disease > Flashcards

The Breadth of GI disease Flashcards

1
Q

a) What is a Mallory Weis Tear
b) How is it diagnosed?
c) How does it present?
d) What two groups of people does it most commonly affect?

A

a) Tear in the lower oesphageal mucosa due to persistant or violent vomiting/retching
b) Endoscopy
c) Hematemesis
d) Alcohol, Pregnancy

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2
Q

a) What is Boerhaave’s Syndrome
b) How does it present?
c) Most common complication

A

a) Transmural laceration of the distal oesophagus due sudden increase in intraesophageal pressure
b) Sudden onset severe chest pain following repeated episodes of vomiting/retching
c) Mediastinitis

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3
Q

What is GORD?

A

When acid from the stomach refluxes through the LES and irritates the lining of the oesophagus

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4
Q

Compare the lining of the stomach vs oesophagus and its relevance to GORD

A

Oesophagus → squamous epithelia making it more sensitive to the effects of stomach acid

Stomach → columnar epithelia that is more protective against stomach acid

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5
Q

What is Dyspepsia?

A

A non-specific term used to describe indigestion

It covers the symptoms of GORD

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6
Q

List 4 symptoms of GORD

(Hint: Horse BARN ♡)

A
  1. Horse voice
  2. Bloating
  3. Acid regurgitation
  4. Retrosternal or epigastric pain
  5. Nocturnal cough
  6. Heartburn
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7
Q

When may you reffer a patient with GORD for an Endoscopy?

Specify whether each is:

  • Admission and urgent endoscopy
  • Two-week-wait referral
A

Admission and urgent endoscopy: Evidence of GI bleed (eg. meleana, coffee ground vomit)

Two-week-wait referral for symptoms suspcious of cancer/ red flags

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8
Q

List 4 red flag features in a patient with GORD indicating referral

A
  1. Dysphagia (any age)
  2. Aged over 55
  3. Weight loss
  4. Upper abdominal pain / reflux
  5. Treatment resistant dyspepsia
  6. Nausea and vomiting
  7. Low haemoglobin
  8. Raised platelet count
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9
Q

List 4 pieces of lifestyle advice you can give a patient with GORD?

A
  • ↓ tea, coffee and alcohol
  • weight loss
  • avoid smoking
  • smaller, lighter meals
  • avoid heavy meals before bed
  • stay upright after meals rather than lying flat
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10
Q

List 3 medication groups for management of GORD

Incl examples

A

Antacids: Gaviscon, Rennie

PPIs: Omeprazole, Lansoprazole

H2 blocker: Ranitidine (alternative to PPI)

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11
Q

Surgical treatment of GORD?

A

Laparoscopic fundoplication

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12
Q

a) What is Achalasia?
b) What age and gender is most commonly affected?

A

a) Failure of oesophageal peristalsis and relaxation of the LOS due to degenerative loss of ganglia from Auerbach’s plexus
b) Middle-age, equal in both genders

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13
Q

a) Swollen, tortuous vessels are called _________ and are a result of _________ due to _________
b) List 4 locations where these can occur?

A

a) varices, portal hypertension, liver cirrhosis

b)

  1. oesophageal varices - GOJ
  2. rectal varicies
  3. anterior abdominal wall via the umbilical vein - caput medusae
  4. Ileocaecal junction
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14
Q

Explain the pathology of Varices

A
  1. cirrhosis ↑ resistance of blood flow in the liver
  2. results in ↑ back-pressure into portal system - “portal hypertension”
  3. back-pressure causes vessels at sites where portal and systemic venous systems anastomose, to become swollen and tortuous
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15
Q

To who and how often is bowel cancer screening offered?

A

Offered every 2 years to men and women between ages of 60 - 74 in the UK using the faecal-immunochemical test (FIT).

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16
Q

Are Varices symptomatic?

A

No, not until they start bleeding

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17
Q

Treatment of stable varices?

A
  1. Propranolol ↓ portal hypertension by acting as a non-selective β-blocker
  2. Elastic band ligation
  3. Injection of sclerosant (less effective than band ligation)
  4. Transjugular Intra-hepatic Portosystemic Shunt (TIPS)
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18
Q

Treatment of bleeding oesophageal varices

A

Resuscitation:

  • Vasopressin analogue - vasoconstrict, slows bleeding
  • Vit K and fresh frozen plasma - correct coagulopathy
  • Broad spectrum antibiotics - prophylactic
  • consider intubation and intensive care

Urgent endoscopy:

  • Sclerosant Injection into varices - to cause “inflammatory obliteration” of vessel
  • Elastic band ligation of varices

Sengstaken-Blakemore Tube (when endoscopy fails) - to tamponade the bleeding varices

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19
Q

What is Portal Hypertensive Gastropathy?

A

Changes in the mucosa of the stomach in patients with portal hypertension (snake skin)

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20
Q

What is Barretts Oesophagus and how does it occur

A

Pre-malignant change in the lower oesophageal epithelium (metaplasia) from squamous to columnar

Due to constant reflux of acid

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21
Q

Barretts Oesophagus is a risk factor for what?

How do we try to prevent this

A

Development of adenocarcinoma of the oesophagus

Monitored by regular endoscopy

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22
Q

Treatment of Barretts Oesophagus

A
  1. PPIs (e.g. omeprazole)
  2. Ablation treatment during endoscopy in patients with dysplasia (destroys epithelium so it is replaced with normal cells)
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23
Q

Is Crohns or UC more prevelant?

A

UC

24
Q

Most common cause of defecation disorders (constipation) in adults and babies

A

Adults: Rectoceles

  • defect in the posterior vaginal wall causes rectum to prolapse forwards into the vagina

Babies: Hirschsprung’s disease

  • congenital condition where nerve cells of Auerbach’s plexus are absent in the distal bowel and rectum
25
Q

Compare internal vs external hemorrhoids

A

Internal: above pectinate line

  • covered by mucus membranes
  • pain fibers have visceral innervation from sympathetic nerves
  • not overly painful
  • more likely to bleed due to ↑ vascularisation

External: below pectinate line

  • covered by skin
  • innervated by afferent somatic pain fibres from the inferior rectal nerves
  • PAINFUL.
26
Q

What is Primary Biliary Cholangitis?

Which part of the liver is first to be affected?

A

Condition where the immune system attacks the small bile ducts within the liver

First part affected tends to be the intralobar ducts (the Canals of Hering)

27
Q

How does Primary Biliary Cholangitis lead to liver failure?

A

Obstruction to the outflow of bile (progressive cholestasis) causes back-pressure which ultimately leads to fibrosis, cirrhosis and liver failure

28
Q

Presentation of Primary biliary cholangitis

A
  1. Extreme fatigue
  2. Itching
  3. Dry skin
  4. Dry eyes
  5. Jaundice

+ abdo pain, pale stools, Xanthoma, signs of cirrhosis and failure (e.g. ascites, splenomegaly, spider naevi)

29
Q

What causes pruritis, jaundice and xanthelasma

A
  1. Bile acids cause itching
  2. Bilirubin causes jaundice
  3. ↑ cholesterol deposits in the skin called xanthelasma (xanthomas are larger nodular deposits in the skin or tendons)
30
Q

Why is primary billary cholangitis associated with an increased risk of CVD?

A

↑ cholesterol depositis on blood vessels

31
Q

a) What age and gender does PBC most commonly affect?
b) What other conditions is PBC associated with?

A

a) Middle aged women

b)

  • Sjogren’s syndrome (upto 80% of patients)
  • RA
  • systemic sclerosis
  • thyroid disease
32
Q

State would be seen in the following diagnostic procedures/investigations for PBC:

a) LFTs
b) Autoantibodies (2)
c) Other blood tests (2)

A

a) ↑ALP in early stages, other liver enzymes and bilirubin raised in later disease
b) Anti-mitochondrial antibodies, Anti-nuclear antibodies
c) ↑ ESR and ↑IgM

33
Q

Treatment of PBC

A
  1. Ursodeoxycholic acid - ↓ intestinal absorption of cholesterol
  2. Colestyramine - binds to bile acids to prevent absorption in the gut
  3. Liver transplant - end stage liver disease
34
Q

What is Primary sclerosing cholangitis?

A

Inflammation and fibrosis of intra and extra-hepatic bile ducts. Results in obstruction to the flow of bile out of the liver and into the intestines

Unknown cause

35
Q

List 4 risk factors for PSC

A
  1. Male
  2. Aged 30-40
  3. Ulcerative Colitis
  4. Family History
36
Q

How does PSC present?

A
  1. Jaundice
  2. Chronic right upper quadrant pain
  3. Pruritus
  4. Fatigue
  5. Hepatomegaly
37
Q

Answer the following for PSC:

a) LFTs
b) Autoantibodies?
c) Gold standard investigation for diagnosis

A

a) ↑ ALP first, ↑ bilirubin as strictures become more severe
b) No Ab are highly sensitive or specific to PSC, but p-ANCA may be positive
c) MRCP (☆) or ERCP - shows multiple biliary strictures, ‘beaded’ appearance

38
Q

What is Hereditary Haemochromatosis

A

Iron storage disorder that results in excessive total body iron and deposition of iron in tissues.

39
Q

What is Wilson’s disease?

What are the 3 ways it may present?

A

Excessive accumulation of copper in the body and tissues

  1. Hepatic problems (40%)
  2. Neurological problems (50%)
  3. Psychiatric problems (10%)
40
Q

How does Wilsons disease affect the liver?

A

Copper deposition in the liver leads to chronic hepatitis and eventually liver cirrhosis.

41
Q

What signs/symptoms would be seen in Wilsons disease?

A

Neurological: dysarthria and dystonia, parkinsonism (tremor, bradykinesia and rigidity)

Psychiatric: range from mild depression to psychosis

Kayser-Fleischer rings in cornea (copper deposition in Descemet’s corneal membrane)

42
Q

How is Wilsons disease diagnosed and treated?

A

Diagnosed:

  • Initial investigation is serum caeruloplasmin (low)
  • Gold standard for diagnosis is a liver biopsy for liver copper content

Treatment: copper chelation

43
Q

What is Alpha-1-antitrypsin and where is it produced?

A

An enzyme which inhibits neutrophil elastase enzyme (digests connective tissues)

Produced in the liver

44
Q

What are the 2 main organs affected by alpha-1-antitrypsin deficiency

A
  1. Liver cirrhosis after 50 years old
  2. Bronchiectasis and emphysema in the lungs after 30 years old
45
Q

What is refeeding syndrome?

A

Occurs in people that have been in a severe nutritional deficit for an extended period, when they start to eat again

Higher risk if BMI < 20 and have had little to eat for past 5 days

46
Q

Pathophysiology behind refeeding syndrome?

List the hallmark electrolyte imbalance

A

In the starved state

  • body turns to fat and protein metabolism
  • there is a ↓ in circulating insulin
  • catabolic state depletes intracellular stores of phosphate

On refeeding levels of insulin ↑ which increases cellular uptake of phosphate (Hypophosphataemia within 4d)

47
Q

List 4 clinical features of refeeding syndrome

A
  1. Rhabdomyolysis
  2. Red and white cell dysfunction
  3. Respiratory insufficiency
  4. Arrythmias
  5. Cardiogenic shock
  6. Seizures
  7. Sudden death
48
Q

How do we prevent refeeding syndrome?

A
  1. Determine hight risk patients
  2. Pabrinex supplement
  3. Start nutritional support under supervision of dietitian
  4. Monitor and correct electrolytes
  5. Restore circulatory volume and monitor fluids and overall clinical status
49
Q

How do we treat refeeding syndrome?

A
  1. Parenteral phosphate administration
  2. Oral supplementation with electrolytes and vitamins (esp Bvitamins and thiamine)
50
Q

What are Schatzki Rings?

A

Circular band of mucosal tissue that can form at the end of the oesophagus, can cause it to narrow

Can cause dysphagia

51
Q

What is a Oesophageal Web?

A
52
Q

What is seen on the image below?

A
53
Q

Are pyloric ulcers most likley to be benign or malignant?

A

Benign, but must always arrange a follow up because an ulcer which doesn’t heal is much more likley to be malignant

54
Q

What is Gastric Antral Vascular Ectasia

A

“Watermelon Stomach”

Condition where BVs in the lining of the stomach become fragile and prone to rupture and bleeding

55
Q

List 4 Therapeutic reasons for doing an endoscopy

A
  1. Stone removal from CBD and PD
  2. Removal of benign and/or malignant lesions
  3. Re-canalisation of blocked lumen
  4. Variceal injections and banding
56
Q

What is Colonic inertia?

A

Inability of the colon to modify stool to an acceptable consistency and move the stool from the cecum to the rectosigmoid area at least once every 3 days

57
Q

List 3 surveillance/ screenING programmes in GI

A
  1. Barrett’s surveillance
  2. Surveillance of IBD and colonic polyps
  3. Bowel cancer screening (50-74 yrs)

Gastrointestinal Block (26 decks)

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