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Clinical scenarios by CBL > GI and Hepatobiliary > Flashcards

GI and Hepatobiliary Flashcards

1
Q

What pathogens are known for causing Liver Abscesses?

A

CASE:
-Coliforms
-Anaerobes
-Staph Aureus
-Enterococci

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2
Q

A patient comes in with a suspected Liver abscess. What are the next steps?

A

1.Take blood cultures
2.Pending culture results start antibiotics
3.Discuss potential drainage with surgeons / interventional radiology

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3
Q

What treatment is given to a patient with a Liver abscess?

A

-IV Gentamicin
-IV Amoxicilin
-IV Metronidazole

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4
Q

If a patient with a Liver abscess has a Penicillin allergy, what can’t be given and what will be given instead?

A

Instead of Amoxicilin give:
IV Vancomycin

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5
Q

A patient comes in with a potential Liver abscess. What other 2 conditions should also be considered?

A

Amoebic abscess or Hyatid Cyst

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6
Q

What are the 3 major forms of liver abscesses?

A

-Pyogenic Abscess - majority of cases, polymicrobial
-Amoebic Abscess- around 10% of cases
-Fungal Abscess - less than 10% of cases

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7
Q

What bacteria causes Amoebic Abscesses?

A

Entamoeba Histolytica

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8
Q

What bacteria causes Fungal abscesses?

A

Candida species

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9
Q

What is the most common cause of Pyogenic Liver disease?

Very key to remember this!

A

Biliary tract disease = obstruction of bile flow facilitates bacterial proliferation.

Examples:
-Biliary stone disease
-Obstructive malignancy affecting the biliary tree
-Strictures
-Congenital diseases

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10
Q

Describe the pathophysiology of Liver Abscesses.

A

1.Infections in organs in the portal bed - for instance systemic bacteremia : e.g Endocarditis and Pyelonephritis
2.Can result in SEPTIC THROMBOPLEBITIS
3.Septic emboli are released into the portal circulation
3.S.emboli are trapped by hepatic sinusoids
4.This is where the microabscesses form
5.The microabscesses coalesce into a solatary lesion

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11
Q

4% of Abscess are caused by what?

A

Fistula formation between local intra-abdominal infections.

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12
Q

What is a fistula?

A

An abnormal opening in the stomach or intestines that allows the contents to leak to another part of the body.

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13
Q

What usually causes an anal fistula?

A

It’s usually caused by an infection near the anus, which results in a collection of pus (abscess) in the nearby tissue. When the pus drains away, it can leave a small channel behind.

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14
Q

List the causes of fistulas in the stomach?

Remember Mneumonic

A

I Rarely Deliver Many Tight Slap SDIMRT
1.Inflammatory bowel disease
2.Radiation
3.Diverticular disease
4.Malignancy
5.Trauma
6.Surgical procedures

Fistulas, think FIST then think SLAP

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15
Q

What is the prognosis of pyogenic liver abscesses?

A

When untreated: Always fatal
With treatment (antibiotics + drainage) : 5-30% of cases are fatal due to SEPSIS, MULTIORGAN FAILURE, HEPATIC FAILURE

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16
Q

What signs would indicate a poor prognosis for a pyogenic abscess?

A

-Multiple Abscesses
-Underlying malignancy
-Severity of underlying medical conditions
-Presence of complications
-Delay of diagnosis

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17
Q

What signs would indicate a poor prognosis for a amoebic abscess?

A

-Bilirubin level > 3.5mg/dL
-Encephalopathy
-Hypoalbuminemia (serum albumin <2g/dL )
-Multiple abscesses

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18
Q

What is the inheritance or transmission of Ornithine Transcarbamylase (OTC) deficiency?

A

It is a genetic condition: X linked recessive

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19
Q

What is the pathophysiology of OTC deficiency ?

A

1.Due to x linked recessive genetic disorder
2.patients have issues processing nitrogen generated from amino acid breakdown in the urea cycle.
3.Results in a build up of ammonia (hyperammonaemia) in the blood
4. which can have serious effects on the CNS
5.Cause vomiting lethargy and coma

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20
Q

What are the symptoms of OTC deficiency?

A

Vomiting, Lethargy and Coma

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21
Q

What is the treatment for OTC deficiency?

A

Nitrogen Scavenging Medication
E.g Oral formulations of benzoate and phenylbutyrate

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22
Q

List the causes of mouth ulcers.

Remember mneumonic

A

Stinky Toads Don’t Infect Little Children

1Stomatitis (Recurrent aphthous ulcers)
2.Trauma
3.Deficiencies of nutrients (e.g B12, folate)
4 .Infections - Viral and fungal (e.g Coxsackie, HIV)
5.Leukoplakia (pre-malignant)
6.IBD (e.g Chron’s)

When thinking mouth ulcers think of toads you kiss with stinky breath

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23
Q

What are Kaposi sarcoma?

i.e Where do you see them and how does it present?

A

Pre-malignant condition of cancer cells in the GI tract, presenting with reddish-blue oral maculae and oral hairy leukoplakia (white patches)

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24
Q

What does Leokoplakia mean?

A

White patches

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25
Q

What is Kaposi Sarcoma caused by? List them.

A

-Epstein-Barr
-Early sign of HIV (the infection is due to immunosuppresion)

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26
Q

What is the management of Kaposi Sarcoma?

A

-No cure for it or Epstein Barr so targets slowing progression and aiding symptoms.

=Highly Active Antiretroviral Therapy (HAART).

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27
Q

What is geographic tongue?

A

Idiopathic inflammation of the mucosa causing loss of papillae, a burning sensation and a map-like appearance (hairy tongue- abnormal proliferation of keratin)

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28
Q

What is the prognosis for Geographic tongue?

A

Pretty harmless and resolves itself.

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29
Q

What does Geographic tongue indicate about a patient?

A

Nothing! Geographic tongue is an independent disorder that is pretty harmless and does not indicate any other pathology.

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30
Q

A patient has dysphagia. How do you decide between the 2 investigative options and what are they?

A

If the patient can’t swallow SOLIDS AND LIQUIDS:

=1.Barium Swallow

If the patient can’t swallow SOLIDS ONLY:

=2.Upper GI endoscopy

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31
Q

What is Achalasia?

A

A motility disorder of the oesophagus causing a lack of propulsion of the oesophagus (aperistalsis) and relaxation of the oesophageal sphincter causing PROGRESSIVE DYSPHAGIA OF BOTH SOLIDS AND LIQUIDS.

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32
Q

What is the pathophysiology of Achalasia?

A

Idiopathic cause of degeneration of the ganglion cells of the myenteric plexus within the oesophageal wall and lower sphincter.

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33
Q

A patient has suspected Achalasia. What are the next steps in diagnosis?

A

1.Barium Swallow Exam
2.CXR
3.Manometry
4.Consider an Upper GI endoscopy

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34
Q

What are possible complications of Achalasia?

A

-Slim associated risk of SQUAMOUS CELL CARCINOMA (SCC) of the Oesophagus
-Oesophageal cancer as a result of long-standing achalasia.

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35
Q

Describe the first line management of Achalasia .

A

First line: Surgical Myotomy (Heller procedure)
+Fundoplication as well for GORD patients / prevent GORD

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36
Q

What is secondary achalasia?

A

Achalasia than can occur for instance, after a compression caused due to a fundoplication surgery.

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37
Q

What are the symptoms of Achalasia?

A

-Dysphagia (SOLIDS AND LIQUIDS)
-Retrosternal pain
-Regurgitation (and can relieve symptoms)

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38
Q

What are the findings of a Barium Swallow Examination of a patient with Achalasia?

A

‘Bird’s Beak’ appearance of the proximal oesophagus as it is dilated and the lower sphincter is narrow.

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39
Q

What findings would suggest Achalasia on a CXR?

A

-Normal
-Widened Mediastinum (due to dilated oesophagus)

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40
Q

What is the gold standard investigation of Achalasia and what would conclude the diagnosis?

A

Manometry
=High resting pressure of the lower oesophageal sphincter

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41
Q

Why is a GI endoscopy sometimes performed for a patient with Achalasia?

A

To rule out malignancy

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42
Q

What is the difference between GORD and Achalasia?

A

Achalasia is dysphagia of SOLIDS and LIQUIDS while GORD is dysphagia of just SOLIDS.

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43
Q

What is the contraindication (s) for first line treatment for Achalasia and what 2 management options are offered instead?

A

-If the patient isn’t fit - the elderly, co-morbidities, bed-bound, palliative etc

1.Endoscopic Pneumatic Dilatation
=Patients who are older and have co-morbidities

2.Botulinum injections into sphincter
=for patients unfit / unwilling for an invasive procedure

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44
Q

Out of all of the management options for Achalasia on offer, what is the less effective?

A

Botulinum injections
=disease frequently reoccurs

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45
Q

What is the difference between Diffuse Oesophageal Spasm and Achalasia?

A

Both are due to dysphagia of SOLIDS AND LIQUIDS but Achalasia is PROGRESSIVE while Diffuse Oesophageal spasm is INTERMITTENT.

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46
Q

What is the key diagnostic tool for a suspect Diffuse Oesophageal Spasm?

A

Barium swallow Examination

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47
Q

What result from diagnostic procedure(s) would you expect from a patient with Diffuse Oesophageal Spasm?

A

‘Corkscrew Oesophagus’

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48
Q

What is the first line treatment for Diffuse Oesophageal Spasm?

A

PPIs e.g Omeprazole

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49
Q

What are the second line treatment options for Diffuse Oesophageal Spasm?

A

Nitrates and Calcium Channel Blockers

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50
Q

What 2 oesophageal disorders mimic anginal attacks?

A

-Diffuse Oesophageal Spasm
-Nutcracker Oesophagus(swallowing contractions are too intense - affects many GORD patients)

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51
Q

What is the final-line management option for Diffuse Oesophageal Spasm?

i.e Last ditch effort

A

Pneumatic Dilatation and Surgical Myotomy

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52
Q

What is a pneumatic dilation?

A

Endoscopic guided procedure to fix restricted oesophageal sphincter by weakening the lower oesophageal sphincter by tearing its muscle fibres by generating radial force.

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53
Q

What is another name for Pharyngeal Pouch syndrome?

A

Zenker Diverticulum

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54
Q

What is Pharyngeal pouch (Zenker Diverticulum)?

A

Rare condition characterised by an outpouching of the oesophagus due to a weakness in the muscle allowing food debris to accumulate which compresses the oesophagus.

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55
Q

What are the symptoms of Zenker Diverticulum?

A

-Progressive Dysphagia
-Regurgitation
-Halitosis

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56
Q

What is Halitosis?

A

Halitosis is an oral health problem where the main symptom is BAD SMELLING BREATH. In most cases, finding the cause of the bad breath is the first step toward treating this preventable condition.

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57
Q

What is the investigation for suspected Pharyngeal Pouch?

A

Barium swallow examination

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58
Q

What is the management of Pharyngeal Pouch?

A

Surgical intervention

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59
Q

What investigation is contraindicated for suspect Pharyngeal Pouch and why?

A

Endoscopy = can perforate the pouch causing complications

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60
Q

What is Dyspepsia?

A

Heart burn and bloating

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61
Q

What are the red flag symptoms associated with Dyspepsia that calls for a further investigation with an Upper Endoscopy?

Remember mneumonic.

A

High SLAM Problem Alert
Haematemesis
Swallowing difficulty
Low Weight
Anorexia
Melaena
Progressive symptoms
Anaemia

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62
Q

What are the 2 causes of GORD?

A

1.Lower Oesophageal Sphincter (LOS) dysfunction which allows acids from stomach but up to oesophagus
2.Hiatus hernia = of the upper stomach which eliminates the natural thoraco-abdominal pressure gradient

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63
Q

What are the 3 classes of hiatus hernias?

A

-Sliding (80%)
-Rolling
-Mixed

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64
Q

What are the risk(s) of Rolling Hernias and what can be done to prevent it ?

A

Increased risk of strangulation
=Repair- Laparoscopic Fundoplication

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65
Q

What lifestyle factors exacerbate GORD?

A

-Smoking
-Alcohol
-Caffeine
-Obesity
-Pregnancy

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66
Q

Describe the pathophysiology of GORD.

A

Relfux of gastric contents into oesophagus exposes the mucosal epithelium to damage and triggers and inflammatory response causing REFLUX OESOPHAGITIS.

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67
Q

What are the symptoms of GORD?

A

-Heartburn (gets worse after meals and after lying down)
-Acid Brash (metallic taste as a result of acid regurgitation)
-Dysphagia
-Atypical chest pain

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68
Q

What are the 3 stages of investigation for a suspect GORD patient?

A

1.PPIs (for young patients / typical symptoms) on a high-dose trial

2.Consider GI endoscopy
=for uncertain diagnosis / patients > 55yrs

3.Consider ambulatory intraluminal pH monitoring
=for patients under consideration for Laparoscopic Fundoplication

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69
Q

Describe what the results of a ambulatory intraluminal pH monitoring from a GORD patient would indicate.

A

pH <4 at >4% of the time would indicate SURGERY

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70
Q

Describe the stepwise management for GORD.

A

1.Lifestyle modification
2.Full dose PPI therapy (4-8 weeks)
3.If symptoms persist / reoccur:
-switch to H2 Antagonist(e.g Cimetidine, ending -tidine)
4.Consider Laparoscopic Fundoplication
(directed according to the pH ambulatory results)

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71
Q

Name 4 complications of GORD.

A

1.Oesophagitis
2.Barret’s Oesophagus
3.Oesophagus Carcinoma
4.Benign Oesophageal stricture

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72
Q

A patient presents with dysphagia (solids only) and vomiting. Other than GORD, what is a key differential to consider?

A

Eosinophilic Oesophagitis

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73
Q

When should a patient with GORD-like symptoms be considered for Eosinophilic Oesophagitis?

A

If they have a history of atopy (e.g ASTHMA, ECZEMA)

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74
Q

What diagnostic procedure would demonstrate Eosinophilic Oesophagitis?

A

Endoscopic Biopsy

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75
Q

What is the treatment for Eosinophilic Oesophagitis?

A

Aerosolised glucocorticoids with oral glucocorticoid therapy in more severe cases.

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76
Q

What is Barret’s oesophagus?

A

Pre-malignant condition due to GORD

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77
Q

How often should a suspect Barret’s Oesophagus be monitored?

A

Endoscopic surveillance every 1-3 yrs

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78
Q

What treatment for HIGH GRADE DYSPLASIA Barret’s oesophagus?

A

Surgical Oesophagectomy

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79
Q

What is the histological definition of Oesophageal cancer and what are the 2 subtypes?

A

Mucosal Neoplasm originating from Oesophageal Epithelium

  1. Squamous Cell Cancer
    2.Adenocarcinoma
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80
Q

What type of cancer does Barret’s Oesophagus usually cause?

A

Adenocarcinoma

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81
Q

Where do the 2 types of Oesophageal cancers originate?

A

-Adenocarcinoma = lower oesophagus *where Barret’s oesophageal changes are

-Squamous Cell Cancer = middle 1/3rd of oesophagus

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82
Q

Describe the prevalence of Oesophageal cancer- is it men or women who are mainly affected?

A

Men twice more than women

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83
Q

What type of Oesophageal Carcinoma is more common in Western Countries?

A

Adenocarcinoma is more common that Squamous Cell Carcinoma

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84
Q

What pre-existing conditions are risk factors of Oesophageal cancer?

A

-GORD
-Barret’s Oesophagus
-Paterson-Brown-Kelly Syndrome

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85
Q

What is Patterson-Brown-Kelly Syndrome?

A

Iron deficiency anaemia being associated with Post-Circoid Webs.

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86
Q

What is another name for Paterson-Brown-Kelly Sydrome?

A

Paterson-Vinson Syndrome

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87
Q

What are Oesophageal webs?

A

An oesophageal web is a thin (2-3 mm), eccentric, smooth extension of normal oesophageal tissue consisting of mucosa and submucosa that can occur anywhere along the length of the oesophagus causing dysphagia.

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88
Q

Is Obesity a risk factor for Oesophageal cancer?

A

Adenocarcinoma:
Risk factor

Squamous Cell Carcinoma:
Protective

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89
Q

What are the symptoms of Oesophageal cancer?

A

-Asymptomatic till late stages:(
-Progressive dysphagia (solids then liquids as well)
-Haematemesis or Melaena
-Late stage Hoarseness
-Weight loss

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90
Q

What are the main risk factors for Squamous Cell Oesophageal carcinoma?

A

Smoking and alcohol

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91
Q

Describe the stepwise investigations for suspect oesophageal cancer.

A

1.Arrange Blood Test (FBC), U&E, LFT
-FBC: Look for anaemia secondary to oesophageal bleed
-Check suitability of CT scan staging
-Look for Liver Metastasis

2.Urgent Oesophagogastroduodenoscopy

3.Staging imaging
-Abdominal CT scan
-PET scan = screens for metastasis

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92
Q

What is the management for the majority of patients diagnosed with Oesophageal cancer and why?

A

70% of patients diagnosed are late stage and therefore metastasis has already happened.

–>Palliative :(
-Chemotherapy and Oesophageal Stenting
=provides symptomatic relief of dysphagia

–>IF PATIENTS ARE FIT:
-Surgical Resection

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93
Q

What is the treatment for Oesophageal webs/ rings?

A

Endoscopic Dilatation or surgery to relieve dysphagia symptoms.

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94
Q

What are the 4 causes of Haematemesis from the stomach?

A

-Peptic / Duodenal Ulcer (NSAID / H.Pylori)
-Gastritis
-Angiodysplasia
-Gastric Cancer

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95
Q

What are the 4 causes of Haematemesis from the oesophagus?

A

1.Varices
2.Oesophagitis
3.Mallory-Weiss Tear
4.Oesophageal cancer

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96
Q

What are the 2 most common causes of upper GI bleeds (Haemetemesis)?

A

Ulcers and Varices

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97
Q

What is the initial resuscitation treatment for a patient in the ER with Haematemesis?

A

1.Ensure Oxygen supply
=High Flow Oxygen
2.Obtain IV access
=Wide-bore canula in each arm
-IV Crystalloid Fluid
3.Send off urgent bloods
-FBCs: Check for anaemia and platelets
-LFTs: Check for pre-existing liver disease
-U&Es : Check existing Acute Kidney Injury and Urea rise
-Clotting and coagulation screen
-Cross match blood

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98
Q

A patient presents with Haematemesis. What does a high urea and normal creatinine suggest?

A

Suggestive of an Upper GI Bleed

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99
Q

What is given to a patient with suspected Variceal bleed?

A

Terlipressin / Octreotide

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100
Q

A patients comes to the ER with Haematemesis. After resecuitation, what are the next steps?

A

Urgent endoscopy

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101
Q

A patient with Haematemesis is considered high risk. What should be given?

A

72hr PPI IV infusion

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102
Q

If haematemesis bleeding continues, what procedures should be considered to stop the bleeding?

A

-Balloon Tamponade
or
-Transjugular Intrahepatic porto-systemic shunting

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103
Q

What is Gastritis?

A

Inflammation of the stomach

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104
Q

What are the 2 types of Gastritis?

A

Acute and Chronic

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105
Q

What are the causes of Acute Gastritis?

A

-H.Pylori Infection
-Alcohol
-NSAIDs/Aspirin
-Stress-induced
-Bile-acid reflux (usually post-op)

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106
Q

What are the causes of Chronic Gastritis?

A

-Chronic H.Pylori
-Chron’s Infection
-Sarcoidosis
-Autoimmune (atrophic)

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107
Q

What does Atrophic mean?

A

Autoimmune

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108
Q

What is the pathophysiology Autoimmune Gastritis?

A

Chronic gastritis caused by autoimmune destruction of the parietal cells of the stomach which means there is an Intrisic Factor deficiency leading to Pernicious Anaemia (B12 deficiency)

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109
Q

What is Pernicious Anaemia?

A

B12 deficiency

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110
Q

The development of Autoimmune Gastritis is strongly associated with WHAT other disorders?

A

3 Endocrine disorders:
-Addison’s
-Type 1 Diabetes Mellitus.
-Autoimmune thyroid disease

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111
Q

What is the treatment for Autoimmune Gastritis?

A

B12 injections and Iron Infusions

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112
Q

What is the treatment for Gastritis?

A

PPIs

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113
Q

List the causes of Peptic Ulcer Disease (recurrent Peptic Ulcers)

A

-H.Pylori
-Drugs -Aspirin / NSAIDs

Secondary to:
-Intracranial neurology
-Burns or ulcer
=Due to this then called CUSHING ULCER

Rare causes:
-Zollinger- Ellison Syndrome
-Chron’s disease

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114
Q

What is a Cushing Ulcer?

A

A peptic ulcer caused by
-Intracranial neurology
-Burns or ulcer

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115
Q

Describe the symptoms of a Peptic Ulcer.

A

-Epigastric pain
-Bloating
-Abdominal distension
-Nausea

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116
Q

Differentiate the stomach pain between a peptic ulcer and a duodenal ulcer.

A

Duodenal ulcer epigastric pain is IMPROVED upon EATING,
while peptic ulcers, epigastric pain get WORSE with EATING

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117
Q

How does H.Pylori cause gastric issues e.g peptic ulcer, gastritis?

A

Stimulated gastrin production as well as inhibiting somatostatin production, resulting in and increase in acid secretion.

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118
Q

A patient with a Peptic ulcer needs to go on NSAID therapy. What else should therefore be prescribed?

A

COX2 inhibitor(e.g Ibeprofen, Naproxen)

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119
Q

A patient has a peptic ulcer due to H.Pylori. What is the management?

A

1.7 day course of Triple Therapy:
-High dose PPIs
-2 twice daily antibiotics
-Amoxicillin
-Metronidazole or Clarithromycin

2.Re-test @ 6-8weeks with Carbon 13 urea breath test

3.Those who remain symptomatic offer Bismuth

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120
Q

If a patient with a H.Pylori Peptic ulcer has a Penicillin allergy, what from their treatment plan must be replaced and what with?

A

Amoxicillin replaced with Clarithromycin

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121
Q

A patient is being prescribed Bismuth. What do they need to be aware of?

A

Expect black stools

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122
Q

What is the management for a peptic ulcer NOT caused by H.Pylori?

A

1.Stop offending medications for 8 weeks
2. Offer medication advice

If recurrent:
-Offer low dose PPI and rule out other reasons

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123
Q

What are possible complications if Peptic Ulcers?

A

-Acute GI haemorrhage
-Perforation causing bleeding into abdominal cavity causing SEVERE PERITONITIS:
MEDICAL EMERGENCY
-Gastric Outlet Obstruction
-Malignant transformation

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124
Q

What type of ulcer is most likely to cause perforation of the ulcer and therefore severe peritonitis?

A

Anterior Duodenal Ulcers

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125
Q

What type of ulcer is more likely to bleed causing peritonitis and why?

A

Posterior Duodenal ulcers (due to their close proximity to the Gastroduodenal artery)

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126
Q

What is meant by Gastric outlet obstruction and what will happen?

A

Gastric outlet obstruction (GOO) is a result of any disease process that causes a mechanical impediment to gastric emptying which then causes Fibrotic Stricturing.

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127
Q

What is Zollinger-Ellison Syndrome?

A

A rare condition caused by gastrin-secreting gastrinoma which is usually pancreatic origin. It is characterised by hypersecretion of GASTRIC ACID, resulting in EXTENSINVE PEPTIC ULCERATION

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128
Q

What is Zollinger-Ellison Syndrome strongly associated with?

A

Multiple Endocrine Neoplasia (MEN TYPE1) which is usually malignant.

Note: 20% of patients with Zollinger-Ellison Syndrome have MEN type 1

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129
Q

What are the symptoms of Zollinger-Ellison Syndrome?

A

-Epigastric pain
(due to ulcerations and GORD)
-Diarrhoea

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130
Q

How does Zollinger-Ellison Syndrome caused Diarrhoea?

A

Due to the high gastric acid secretion, this damages pancreatic enzymes that are required in the small intestine and therefore damages it leading to incomplete digestion and therefore Diarrhoea

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131
Q

What investigations are necessary for suspect Zollinger-Ellison Syndromeand what would the results be?

A

1.FBC
=Microcytic anaemia due to chronic ulcer bleed
2.Fasting gastrin levels
>1000pg/ml is diagnostic
3.MEN1 Screen (Calcium, PTH and Prolactin)
4.Endoscopic ultrasound
=check for cancer and metastasis

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132
Q

What is the treatment for Zollinger-Ellison Syndrome?

A

First line: High dose PPIs
Localised diseases (some need): Surgical resection
If Metastatic: Somatostatin analogues

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133
Q

What type of cancer is usually gastric cancer?

A

Adenocarcinoma

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134
Q

How is more likely to get gastric cancer, men or women?

A

Men (twice as much)

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135
Q

What lifestyle factor links Japan to Gastric Cancer more than Western countries?

A

Raw fish diet

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136
Q

What other disorders are risk factors of Gastric Cancer?

A

-Autoimmune Gastritis
-Familial Adenomatous Polyposis

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137
Q

What are the symptoms of Gastric Cancer?

A

-Usually asymptomatic in early stages
-Dyspepsia
-Progressive dysphagia with vomiting and haematemesis
-Weight loss /Anorexia
-Iron-deficiency anaemia

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138
Q

What is Linitis Plastica?

A

Rare form of diffuse gastric cancer that has a leather bottle appearance and is NOT caused by H.Pylori.

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139
Q

What are Eponymous signs?

A

-Supraclavicular nodes metastasis (Virchow’s sign)
-Umbilicus metastasis
-Ovaries metastasis

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140
Q

What is a Virchow’s node?

A

Metastasis to Supraclavicular nodes

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141
Q

What is Sister Joseph nodules?

A

Umbilicus metastasis

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142
Q

What is a Krukenberg tumour?

A

Ovaries metastasis

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143
Q

Describe the stepwise investigations into suspected gastric cancer.

A

1.FBC: Microcytic anaemia
2.LFTs (Liver metastasis?)
3.Urgent upper GI endoscopy
-CT, AXR and Pelvis (for staging)

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144
Q

How to treat early-localised Gastric Cancer?

A

Curative Surgical Resection with pre-operative neoadjuvant chemotherapy

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145
Q

How to treat advanced non-operable gastric cancer?

A

Palliative
-Chemo
-Stenting

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146
Q

What is the treatment for Human Epidermal Receptor 2 positive metastatic disease?

A

Trastuzumab

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147
Q

What are Gastrointestinal Stromal Tumours?

A

Submucosal tumours originating from the Interstitial cells of Cajal.

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148
Q

What is the treatment for Gastrointestinal Stromal Tumours?

A

Imatinib

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149
Q

What antibiotics are used for Clostridium Difficile Colitis?

A

Non-severe:
10-14day course of oral Metronidazole
-Severe:
IV Metronidazole and Oral Vancomycin

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150
Q

A patient has been diagnosed with Clostridium Difficile Colitis. What are the next steps in order of priority?

A

1.INFECTION CONTROL
=isolated to side room with barrier and nursing precautions
2.STOP ALL CAUSATIVE AGENTS AND:
-Antibodies
-PPIs
3.ANTIBIOTIC THERAPY
-Non-severe:10-14day course of oral Metronidazole
-Severe:IV Metronidazole and Oral Vancomycin
4.CONSIDER SURGERY
=Only in fulminant disease (SUDDEN AND SEVERE ONSET)

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151
Q

What COULD come up on an AXR for a patient with suspected Clostridium Difficile Colitis?

A

Colonic dilatation
i.e >6cm

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152
Q

What blood results and U&E results would you expect from a patient with Clostridium Difficile Colitis?

A

Blood–>
INCREASE:
-White blood cells
-CRP

DECREASE :
-Albumin

U&E–>
DERRANGED
(due to dehydration)

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153
Q

A patient presents with watery stool and colic abdominal pain as well as a fever. What tests in what order would you like to do?

A

1.Arrange FBC
2.Stool testing
3.AXR
4.Consider colonoscopy

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154
Q

Describe the pathophysiology of Clostridium Difficile Associated Disease.

A

1.Clostridium Difficile bacteria produces ENTEROTOXINS A and B
2.Triggers inflammatory process
3.Leads to vascular permeability and pseudomembrane formation

=(Accumulation of inflammatory cells, fibrin and necrotic debris which contributes to the pseudomembrane)>

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155
Q

What are the symptoms of a patient with Clostridium Difficile Associated Disease?

A

-Profuse WATERY diarrhoea
-Colic abdominal pain
-Fevers
-Rigors

NOTE: Sever abdominal pain is NOT common with this

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156
Q

How long after the start of an antibiotic treatment can Clostridium Difficile Colitis occur?

A

5-10 days after

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157
Q

What antibiotics are known for causing Clostridium Difficile Colitis?

A

‘C’ Antibiotics
1.Co-Amoxiclav
2.Cephalosporins
3.Clindamycin

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158
Q

What is Clostridium Difficile Associated Disease?

A

Gram Positive, Anaerobic, Spore Forming Bacterium that lie dormant in 3-5% of the population and is AWAKENED by certain antibiotics that can cause PSEUDOMEMBRANOUS COLITIS

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159
Q

What is the prognosis for most Gastroenteritis cases?

A

SELF-LIMITING infection

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160
Q

List the common causative agents of Gastroenteritis?

A

-Bacterial: Campylobacter, E.Coli, Salmonella

-Viral (30-40%): Norovirus and Rotavirus

-Parasites: Giardiasis, Cryptosporidiosis

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161
Q

What is meant by Gastroenteritis?

A

NON-SPECIFIC term used to characterise 4 symptoms together:
-ACUTE Diarrhoea
-Nausea
-Vomiting
-Abdominal pain

Loosely associated with Infective Diarrhoea.

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162
Q

What is Coeliac Disease?

A

Autoimmune disorder triggered by gluten resulting in small bowel inflammation and subsequent malabsorption

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163
Q

What haptotype is Coeliac disease related to (90% of patients have it) and is presented on APC cells

A

HLA-DQ2

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164
Q

What are APC cells (Antigen Presenting Cells) responsible for?

A

Inflammation cascade

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165
Q

What are the 4 classes of symptoms you would expect to see in a patient with Coeliac’s Disease?

A

-GI complaint
-Metabolic (deficiencies)
-Dermatological
-Associated conditions

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166
Q

What GI symptoms could a patient with Coeliac’s present with?

A

-Abdominal pain
-Steatorrhoea (fat droplets in stool)
-Flatus
-Unexplained weight loss

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167
Q

What does Steatorrhoea mean?

A

It is an increase in fat excretion in the stools which indicates fat malabsorption .

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168
Q

What conditions could be responsible for Steatorrhoea?

A

Exocrine pancreatic insufficiency (EPI), coeliac disease, and tropical sprue

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169
Q

What metabolic presentation can you see in a patient with Coeliac’s Disease?

A

-Iron (MICROCYTIC ANAEMIA), B12 and folate deficiency (PERNICIOUS ANAEMIA, EPILEPSY)

-Hypocalcaemia (TENTANY, OSTEOMALACIA, OSTEOPOROSIS)

-Failure to grow/thrive as a child

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170
Q

How can a patient with Hypocalcaemia present?

A

With Tetany, Osteomalacia or Osteoporosis

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171
Q

What is Tetany?

A

It is involuntary contractions of muscles due to low calcium.
Common symptoms of tetany:
-numbness around the mouth
-muscle cramps
-paresthesias affecting the hands and feet.

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172
Q

What dermatological condition affects patients with Coeliac?

A

Dermatitis Herpetiformis

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173
Q

What conditions are associated with Coeliac?

A

Autoimmune:
-Type1 Diabetes
-Thyroid Disease
-Primary Biliary Cholangitis

Cancer:
-Lymphoma, Breast, Small Bowel

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174
Q

What percentage of Coeliac patients have Dermatitis Hepetiformis?

A

20%

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175
Q

Describe Dermatitis Hepetiformis.

A

Pruritic (ithcy),Vesicular rash affecting mainly the EXTENSOR surfaces due to deposition of IgA complexes in the Dermis.

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176
Q

What is the treatment for Dermatitis Herpetiformis?

A

Usually a gluten free diet but in resistant cases

=DAPSONE

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177
Q

What is tested for in serological testing for a patient with suspected Coeliac’ s Disease?

A

IgA Autoantibodies:

-Anti-endomysial
-Anti-Gliadin
-Anti-tissue transglutaminase (tTG)

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178
Q

Other than serological testing, what is the gold standard diagnostic test for Coeliac’s Disease?

A

Duodenal Biopsy

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179
Q

What are the 2 main findings on a Duodenal Biopsy from a patient with Coeliacs?

A

-Subtotal villous atrophy
-Lymphocyte infiltration of laminal propria

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180
Q

What electrolytes are imbalanced in Coeliac’s disease?

A

Decreased:
-Calcium
-Magnesium
-Albumin

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181
Q

What is Refractory Coeliac’ s Disease?

A

Is defined by persistent or recurrent malabsorptive symptoms and villous atrophy despite strict adherence to a gluten-free diet (GFD) for at least 6–12 months in the absence of other causes of non-responsive treated coeliac disease (CD) and overt malignancy.

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182
Q

What additional management should considered in a patient with Refractory Coeliac’ s Disease?

A

Prednisolone

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183
Q

What underlying conditions can causes Refractory Coeliac’ s Disease?

A

-Small Intestinal bacterial overgrowth
-IBD =Chron’ s and Ulcerative Colitis
-Irritable Bowel Disease = common idiopathic irritation of digestive tract causing abdominal cramps, diarrhoea and constipation

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184
Q

What is another name for Small Intestine Bacteria Overgrowth (SIBO)?

A

Blind Loop Syndrome

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185
Q

What causes Small Intestine Bacteria Overgrowth?

A

Increase of bacteria in small bowel caused by:

-Long standing PPI therapy
-Post-Gastrectomy
-Scleroderma
-Diabetic Gastroparesis
-Post-bowel resections (blind loops)
-Small bowel Diverticulosis
-Small Bowel Obstruction

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186
Q

What is Diabetic Gastroparesis?

A

Nerve damage due to glucose causing issues with contractions with the stomach

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187
Q

How is the diagnosis of Small Intestine Bacterial Outgrowth confirmed and why?

A

By Hydrogen breath test AFTER a meal

BECAUSE: Bacteria metabolises glucose into hydrogen, so after a meal there would be high hydrogen in a patient with SIBO.

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188
Q

What is the management for Small Intestine Bacterial Outgrowth?

A

-Treat underlying cause
-Cyclic regime of antibiotics:
-Doxycycline
-Rifaximin
-Metronidazole

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188
Q

What is Tropical Sprue?

A

Progressive disorder of malabsorption due to most likely an infectious cause that is ripe in Far East and South America.

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188
Q

What is the management for Tropical Sprue?

A

-Often improve by itself but IF PROLONGED:
–4 week course of Tetracyclines

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188
Q

What does the histological features of a patient with Tropical Sprue look like?

A

Same as the histology for Coeliac’ s disease

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189
Q

What is Whipple’s Disease?

A

Rare and chronic infectious malabsorption disease causing multi-systemic effects.

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190
Q

Who is most likely affected by Coeliac’ s Disease- men or women?

A

Women

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191
Q

What bacteria causes Whipple’s disease?

A

Gram positive bacterium:
=Tropheryma Whipplei

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192
Q

Who is the typical Whipple’s disease patient?

A

Middle-aged Caucasian Men

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193
Q

What are the symptoms of Whipple’s disease?

A

First present with :
-Arthralgia (pain in joint)
-Progressive Weight Loss

Late presentation:
-Diarrhoea

Occasionally can see:
-Neurological symptoms (e.g Demetia, Myoclonus)

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194
Q

What does Arthralgia mean?

A

Pain in 1 joint

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195
Q

How do you diagnose a patient with Whipple’s Disease?

A

By BIOPSY

=Presence of periodic acid-Schiff (PAS) positive MACROPHAGES

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196
Q

What is the treatment for Whipple’s disease?

A

-IV antibiotics for 2 weeks
-Followed by Oral Co-Trimoxazole

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197
Q

A patient with Chron’s disease has had a surgical resection but is now suffering from diarrhoea. What could this indicate?

A

Short Bowel Syndrome
(extensive bowel failure usually due to surgical complication)

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198
Q

What percentage of tumours are in the small intestine?

A

4%
SI cancer is NOT common

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199
Q

What type of malignant tumours are the most common in the small intestine?

A

Adenocarcinomas

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200
Q

What are the causes of Adenocarcinomas in the small intestine?

A

Familial Adenomatous Polyposis (heretidary) or Chron’s disease.

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201
Q

What are the investigations for Adenocarcinomas in the small intestine?

A

-Capsule Endoscopy
-CT imaging

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202
Q

What is the management for Adenocarcinomas in the small intestine?

A

Surgical resection

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203
Q

Where do Adenocarcinomas of the small intestine usually arise?

A

Peri-ampullary region of DESCENDING DUODENUM

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204
Q

Where do Lymphomas of the small intestine originate?

A

Ileum

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205
Q

What types of patients are more susceptible to Lymphomas of the small intestine?

A

-Immunocompromised patients (HIV, medications)
-Coeliac Disease

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206
Q

What are the main symptoms of Lymphomas of the small intestine?

A

Abdominal pain and obstructive symptoms

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207
Q

What are obstructive symptoms of the small bowel?

A

Abdominal pain, cramping or bloating.
Nausea and vomiting.
Lack of appetite.
Malaise (an overall feeling of illness).
Diarrhea (usually a sign of a partial blockage).
Rapid heartbeat, dark-colored pee (urine) and other signs of dehydration.

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208
Q

What are obstructive symptoms of the large bowel?

A

Cramping, abdominal pain, vomiting and inability to pass bowel motions (faeces or poo) or gas

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209
Q

Where do Carcinoid tumours of the small intestine originate?

A

Terminal ileum and appendix

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210
Q

What are the symptoms of a patient with Carcinoid tumour of the small intestine ?

A

-Obstructive symptoms (diarrhoea, cramping, nausea etc)
-Systemic Symptoms (fever, fatigue, body ache)

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211
Q

What is Carcinoid Syndrome?

A

Occurs in 10% of patients with Carcinoid tumours and usually only in the presence of LIVER METASTASIS and is due to an increase in ectopic secretions of SERATONIN

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212
Q

What are the symptoms of Carcinoid syndrome?

A

-Facial flushing
-Chronic Diarrhoea
-Wheezing
-Palpitations
-Abdominal pain

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213
Q

What is the management of Carcinoid Syndrome?

A

Surgical resection

-can also have somatostatin analogues (e.g Octreotide, Lanreotide)

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214
Q

Give 2 examples of Somatostatin analogue medications.

A

ending -reotide

1.Octreotide
2.Lanreotide

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215
Q

What age group is affected by Ulcerative Colitis?

A

Bimodial distribution of onset:
15-30
OR
55-65

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216
Q

What are the symptoms of Ulcerative colitis?

A

-Blood diarrhoea
-Colicky abdominal pain
-Tenesmus (passing motion and not feeling complete)

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217
Q

What are the extra-abdominal manifestations of ulcerative colitis and chron’s?

(Remember meumonic)

A

Antonio Always Races Grand Prix At Every Parade

-Ankylosing Spondylitis
-Arthiritis
-Renal stones
-Gallstones
-Primary Sclerosing Cholangitis
-Anterior Uveitis (red sclera)
-Erythema Nodosum
-Pyoderma Gangrenosum

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218
Q

What investigations must be done for a suspect ulcerative colitis?

A

-FBCs
-Stool testing (rule out cancer and check for Faecal Calprotectin)
-AXR
-Sigmoidoscopy

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219
Q

When would you do a colonoscopy in suspect Ulcercative colitis?

A

You don’t! Can complicate this= high risk of perforation

USE a SIGMOIDOSCOPY instead

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220
Q

What is the management of severe remission of Ulcerative Colitis?

A

1.Urgent hospital admission
2.IV Corticosteroids / Cyclosporin
3.VTE Prophylaxsis
4.Add IV Cyclosporin if unresponsive still
5.Consider urgent surgery

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221
Q

What is the management of mild-moderate remission of Ulcerative Colitis?

A

1.Aminosalicylates (e.g Mesalazine)
2.+Oral Corticosteroids (if contraindicated first line or still no improvement)
3.+Tacrolimus (if still unresponsive)
4.Consider if still unresponsive:
-Adalimumab
-Golimumab
-Vedolizumab

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222
Q

What is the management for maintaing remission of Ulcerative Colitis?

A

-Oral/Topical Aminosalicylates
-IF VERT SEVRE:
Consider: Azathioprine or Mercatopurine
-IF CHRONICALLY SYMPTOMATIC
Consider: Elective surgery

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223
Q

What does Ulcerative colitis affect?

A

The rectum and extends proximally

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224
Q

What does Chron’s disease affect?

A

Transmural anywhere in the GI tract

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225
Q

Who is more likely to have Chron’s - males or females?

A

Females

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226
Q

Give an example of an Aminosalicylate?

A

Mesalazine

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227
Q

What are the symptoms of Chron’s?

A

-Not usually bloody
-Abdominal discomfort
-Weight loss
-Apthous ulcers
-Glossitis

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228
Q

What is management for Chron’s?

A

1.Oral/IV Corticosteroids

2.Budesonide / 5A Therapy
=In patients with distal ileal or right sided colonic disease

3.Azathioprine in resistant cases

4.Infliximab or Adalimumab
=if patients are unresponsive to treatment

5.Consider surgery
=In patients with localised distal ileal disease

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229
Q

A patient with Chron’s is resistant to their medications. What next step should be considered, what should be done before this and why?

A

-Adding or swapping to AZATHIOPRINE

-Do a TIOPRINE METHYLTRANSFERASE levels check

-10% of people have lowered TMT levels which puts them at risk of thiopurine toxicity.

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230
Q

What are the symptoms of Thiopurine Toxicity?

A

Neutropenia: Less neutrophils in body
-Hypersensitivity Reactions
-Marrow suppression
-Pancreatitis

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231
Q

A patient with Chron’s is affected in a localised distal ileum. What is the management?

A

Surgery

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232
Q

What is the management in patients with distal ileal or right sided colonic disease

A

Budesonide / 5A Therapy

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233
Q

What is the most important lifestyle change for a patient with Chron’s?

A

Stop smoking

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234
Q

What complications of Chron’s need to be monitored for?

A

-Osteopenia
-Osteoporosis
-Colorectal surveillance (for patients with Chron’s for 10 years plus)

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235
Q

What is the management for Perianal Chron’s disease?

A

Oral antibiotics:
-Metronidazole / Ciprofloxacin

Fistula healing:
-Azathioprine and maybe Infliximab

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236
Q

What is Microscopic Colitis?

A

Form of IBD that only affects the colon and rectum.

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237
Q

What is the main symptom of Microscopic Colitis?

A

Watery Diarrhoea

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238
Q

What is microscopic colitis associated with?

A

Rheumatoid Arthiritis, Coeliac Disease, NSAID and PPI usage

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239
Q

What is the treatment for Microscopic Colitis?

A

Steroids

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240
Q

What medications can be used to treat symptoms of IBS?

A

-Anti-spasmodics
-Laxatives
-Antimotility Agent (Loperamide)

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241
Q

What 3 diseases does Ischaemic Bowel Disease refer to?

A

1.Acute Mesenteric Ischaemia
2.Chronic Mesenteric Ischaemia (intestinal angina)
3.Ischaemic Colitis

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242
Q

What does Postprandial mean?

A

After a meal

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243
Q

What are the clinical features of Ischaemic Bowel Disease?

A

Occlusive Disease:
-Association with ATRIL FIBRILLATION
-Primary Atherosclerosis
-Distal embolism etc

Non-Occulsive
-Septic shock
-Hypoperfusion

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244
Q

What are the symptoms of Ischaemic Bowel Disease?

A

-SEVERE AND CONSTANT Coliky abdominal pain
-Peritonism (a redness and swelling (inflammation) of the lining of your belly or abdomen.)

245
Q

What is a specific symptomatic feature of Chronic Mesenteric Ischaemia?

A

Post-prandial (after meal) pattern of symptoms

246
Q

What is the gold standard investigation for Ischaemic Bowel Disease?

A

CT Angiogram

247
Q

What should urgently be done if Ischaemic Bowel Disease is suspected?

A

ABG with lactate analysis

248
Q

What would you expect from a lactate analysis from a patient with Ischaemic Bowel Disease?

A

High Lactate ~ Cell Hypoxia

249
Q

What is the management for Ischaemic Bowel Disease?

A

1.Fluid Resuscitation
2.Empirical antibiotics
3.Anticoagulation
4.Surgery if severe

250
Q

What is Diverticular Disease?

A

Inflammation of the Diverticula (outpouching of the mucosa through the muscular wall with the peritoneum still intact).

251
Q

What is a Diverticulum?

A

Outpouching of the mucosa through the muscular wall with the peritoneum still intact in the intestines.

252
Q

What is Colonic Diverticula?

A

Saclike pouch of colonic mucosa and submucosa that protrudes through the muscular layer of the colon; because it does not contain all layers of the bowel, it is considered a pseudodiverticulum

253
Q

What is the prevalence of Diverticulitis?

A

-50% of people affected by age 50
-70% of people affected by age 80

254
Q

What type of diverticulitis is most prevalent in Western Countries and what is most common in Asian countries?

A

West:
=Left sided i.e Descending and Sigmoid colon

Asia:
=Right sided i.e usually congenital

255
Q

How is right sided diverticulitis different from left?

A

Usually is congential

256
Q

How does right sided diverticulitis present?

A

Similar presentation to appendicitis.
-Fulminant pain in lower right abdominal quadrant
-Pain that worsens with coughing, walking or making other jarring movements.
-Nausea and vomiting.
-Loss of appetite.

257
Q

What part of the intestine is most affected by Diverticulitis and why?

A

Sigmoid colon
BECAUSE of its smaller diameter, it makes it more susceptible to more strain and pressure.

258
Q

What are the symptoms of Diverticulitis?

A

Most are asymptomatic:
-Altered bowel habit
-Left Iliac Fossa pain
-Pryrexia (fever)
-Abrupt intermittent perirectal bleeding occasionally

259
Q

What is the pathophysiology of Diverticulitis?

A

1.Low Fibre diet predisposed patient to an INCREASE OF INTESTINAL TRANSIT TIME
2.This REDUCED STOOL VOLUME
3.A reduction of stool volume requires HIGHER INTRALUMINAL PRESSURE to allow bowel movement
4.This WEAKENS AREA (particularlly between tenia coli) which makes it Susceptable to HERNIATION AND DIVERTICULA FORMATION

260
Q

What findings would you expect from testing for Diverticulitis?

A

Blood test:
-Increased White blood cells
-CRP may be present

AXR/CXR:
Pneumoperitoneum

Endoscopy:
No signs of colorectal cancer

261
Q

A patient has suspected diverticulitis. What 2 procedures should therefore be avoided?

A

-Enemas
-Colonoscopy

=can perforate the diverticula (pouches)

262
Q

A patient has asymptomatic diverticulitis. What is the management?

A

-High Fibre Diet
-Laxatives (for constipation)

263
Q

A patient has mild diverticulitis. What is the management?

A

-Oral hydration and bowel rest
-7day course of co-amoxiclav and metronidazole

264
Q

A patient has severe diverticulitis. What is the management?

A

-Admitted to hospital and NBM (Nothing By Mouth)

-IV fluids, analgesia and supportive therapy

-IV antibiotics (e.g cefazolin, cefuroxime, or ceftriaxone)

-Consider surgery

265
Q

What are the 3 common IV antibiotics used for severe diverticulitis?

A

Cefazolin
Cefuroxime
Ceftriaxone

266
Q

What are the 4 main complications of Diverticulitis and what is their management?

A

1.Perforation : Urgent Surgical Resection
2.Major Haemorrhage : Radiologically guided embolism
3.Abscess : IV antibiotics and drainage
4.Strictures : Surgical Resection or Stent insertion

267
Q

How common are colonic polyps and in what age bracket in the west?

A

50% of over 60yr olds

268
Q

A patient has a routine colonoscopy and an adenoma is found. What is it, what should be done and what does this put this patient at risk of?

A

-Most common type of polyp
-Removed immediately
-Colorectal cancer

269
Q

A patient has a polyp removed. What is the monitoring and what is it for?

A

Colonoscopy ever year if more than 5 polyps removed and ever 5 years if only 1-2 removed.

=Monitoring for Colorectal cancer

270
Q

What is the inheritance of Familial Adenomatous Polyposis (FAP) and what is the mutation?

A

Autosomal dominant, APC gene chromosome 5

271
Q

What are the 2 main Familial Adenomatous Polyposis (FAP) variants?

A

1.Gardener’s Syndrome
+thyroid tumours, osteomas and supernumerary teeth

2.Turcot syndrome
+CNS tumours

272
Q

What is a very common complication of Familial Adenomatous Polyposis (FAP) if untreated?

A

90% will develop cancer

273
Q

What is Familial Adenomatous Polyposis (FAP) ?

A

Genetic disorder causing hundreds - thousands of polyps in the colon to rectum (also can be in SI and stomach)

274
Q

What is the management of Familial Adenomatous Polyposis (FAP) ?

A

-Prophylactic Colectomy (removal of part of the colon to reduce cancer risk)
-First degree relatives to be offered genetic testing

275
Q

What is the general age of onset of Familial Adenomatous Polyposis (FAP) ?

A

15yrs

276
Q

What is the inheritance of Hereditary Non-Polyposis Colon Cancer (HNPCC)?

A

Autosomal dominant

277
Q

What is the mean age of onset of Hereditary Non-Polyposis Colon Cancer (HNPCC) ?

A

40yrs

278
Q

What is the Amsterdam criteria (i.e the criteria to diagnose Hereditary Non-Polyposis Colon Cancer (HNPCC)) ?

A

3,2,1 rule:
>3 family members affected with more than 1 of those being a first degree relative
>2 Generations are affected
>1 family member under the age of 50 was diagnosed with Colon cancer

!FAP must be excluded

279
Q

What is Hereditary Non-Polyposis Colon Cancer (HNPCC)?

A

Genetic disorder causing adenomas in the right side of the colon as well as concurrent tumours (breast, ovaries, bladder, stomach and endometrium)

280
Q

What is the presentation for right-sided colorectal cancer?

A

-Bleeding and anaemia
-Constipation
-late obstruction
-colicky abdominal
-weight loss

281
Q

What is the presentation for left-sided colorectal cancer?

A

-fresh rectal bleeding
-loose stools
-early obstruction

282
Q

What are the general options for managing colorectal cancer?

A

-Chemo/Radio
-Laparoscopic surgical resection

283
Q

What is management of anal fissures?

A

-Laxatives
-Topical GTN or Calcium channel blockers (reduces hypertonicity of the anal sphincter)

284
Q

A patient presents with extreme pain and is unable to sit with anal discharge and occasional pyrexia (fever). What could this be and what would you do?

A

Anorectal abscess / fistulae
=surgical drainage and antibiotics

285
Q

What antibiotics are commonly used to treat anorectal abscesses?

A

Cefadroxil, Cefazolin, Cefixim, Cephalexin

286
Q

What are the causes of Pancreatitis?
Remember mneumonic

A

GET SMASHED

Gallstones
Ethanol
Trauma

Steroids
Mumps and infections
Autoimmune
Scorpian Venom
Hyperlipidaemia / Hypercalcaemia
ERCP-induced
Drugs - Azathioprine, Diuretics, Valproate

287
Q

What 3 drugs that can cause Pancreatitis?

A

Azathioprine, Diuretics, Valproate

288
Q

What is the presentation of Pancreatitis?

A

-Severe EPIGASTRIC pain that can radiate to the back sometimes characterised as a tight band of pain encircling the abdomen

-Tachycardia

-Pyrexia

-Hypoxia

-Severe cases: Cullen and Grey-turner sign

289
Q

What is the Cullen sign?

A

Peri-umbilical discolouration
(Pancreatitis)

290
Q

What is the Grey-Turner’s sign?

A

Flank discolouration
(Pancreatitis)

291
Q

What is the pathophysiology of Pancreatitis?

A

Premature intra-pancreatic activation of digestive enzymes causes autodigestion of the Pancreas itself.

292
Q

What results would you expect from a blood test for a patient with Pancreatitis?

A

-Elevated amylase or lipase
-Elevated White blood cells
-Elevated CRP
-LFT would show obstruction (High ALP and GGT)

293
Q

What defines severe pancreatitis?

A

CRP >150 after 48hrs of symptoms

294
Q

What investigations should be done for a suspected case of pancreatitis?

A

-FBC
-U&Es
-LFT
-CT abdomen

295
Q

A patient is admitted to hospital with Pancreatitis. What should be done for initial resuscitation?

A

-O2 (prevent hypoxia)
-Nil by mouth, Insert NG tube
-Analgesia
-Anti-emetics (for the nausea and vomiting)
-IV fluid replacement (Isotonic Crystalloid fluids)
-Monitor fluid balance
-VTE Prophylaxis
-ERCP (if there is also gall stones)

296
Q

What should be done after 2 weeks of a patient having Pancreatitis?

A

Urgent Laparoscopic Cholecystectomy

(to prevent reoccurrence since the reoccurrence chance is 80%)

297
Q

What are the systemic complications that can happen within 7days of a patient having Pancreatitis?

A

1.Respiratory- Pleural Effusion
2.CV- Hypovolaemic
3.Haematology- Disseminated Intravascular Coagulopathy
4.Renal - Renal Failure

298
Q

What is the mean age of onset for Pancreatitis?

A

60s

299
Q

What is Pancreatitis?

A

Acute inflammation of the exocrine pancreas as a result of acute insult.

300
Q

What is the main cause of Chronic Pancreatitis?

A

Alcohol abuse

301
Q

What is the difference between acute and chronic pancreatitis?

A

Acute is often self-limiting and chronic is irreversible damage

302
Q

What is Chronic Pancreatitis characterised by?

A

Recurrent abdominal pain and progressive destruction of the exocrine pancreas.

303
Q

Give examples of common anti-emetics and what do they do?

A

Treat nausea and vomiting

Metoclopramide (Reglan), Domperidone (Motilium), and Chlorpromazine,

304
Q

What is Steatorrhea?

A

Excessively oily stool

305
Q

What are the symptoms of Chronic Pancreatitis?

A

-Intermittent upper abdominal pain radiating to the back
-Associated nausea / vomiting
-Malabsorption
=Steatorrhea or Diarrhoea, Decreased appetite and Weight Loss

306
Q

A patient has suspected Chronic Pancreatitis. What investigations are necessary?

A

-CT of pancreas
-Pancreatic function

307
Q

A patient has suspected Chronic Pancreatitis. What would you expect their pancreatic function to be?

A

-Serum glucose may be elevated
-Faecal Elastase will be reduced

308
Q

What is the management for Chronic Pancreatitis?

A

-Alcohol cessation
-Low fat diet
-Analgesia (NSAIDs)
-Supplements: Creon, Vit A,D,E and K
-PPI
-Glycaemic control

309
Q

What symptoms would indicate cancer of the head of pancreas?

A

Painless jaundice and a palpable non-tender gall bladder

Other general symptoms include:
-Epigastric pain
-Unexplained weight loss

310
Q

What is the main risk factor for Pancreatic Cancer?

A

Smoking

311
Q

A patient has painless jaundice and non-tender enlarged gall bladder, what investigations should be done and why?

A

Suspected Pancreatic Cancer

1.Abdominal Ultrasound
2.CT
3.Histology
4.CA19-9 tumour markers

312
Q

What is the main treatment for a patient with Pancreatic Cancer?

A

Whipple Procedure and adjuvant chemotherapy

313
Q

What is the palliative management (metastasis) for Pancreatic Cancer?

A

First line for metastasis:
Paclitaxel or Gemcitabine

314
Q

A patient presents with crampy abdominal pain. On exam everything seems normal and seems to be due too smooth muscle spasms. What would be prescribed and what are the common side effects?

A

Hyoscine butylbromide

=Constipation and decrease of urination

315
Q

What urine results would you expect for Pre-Hepatic causes of Jaundice?

A

-No bilirubin
-Increased urobilinogen

316
Q

What urine results would you expect for Hepatic causes of Jaundice?

A

Increased Bilirubin and Urobilinogen

317
Q

What urine results would you expect for Post-Hepatic causes of Jaundice?

A

-Increased Bilirubin
-No Urobilogin

318
Q

What LFT results would you expect for Pre-Hepatic causes of Jaundice?

A

-Increased unconjugated Bilirubin
-Increased LDH (indicated Haemolysis)

319
Q

What is a ‘Hepatic Picture’?

A

Increased AST and ALT (with AST being wayyy higher)

Note: GGT and ALP can also be high but if AST and ALT are much higher you know its Hepatic cause of Jaundice.

320
Q

What is a ‘Cholestatic/ Obstructive Picture’?

A

VERY high Unconjugated Bilirubin

-HIGH ALP and GGT (much higher than AST and ALT)

321
Q

What can a solo increased GGT mean?

A

GGT = excessive alcohol consumption

322
Q

What can a solo increased ALP mean?

A

Bone issues e.g Paget’s Disease

323
Q

What does Pre-Hepatic mean?

A

1.Haemolysis
-Haemolytic anaemia
-Thalassaemia
-Malaria
-Drugs-antimalarials

2.Gilbert’s Syndrome

324
Q

What does Hepatic mean?

A

1.Hereditary
-Haemochromatosis
-Wilson’s Disease
-Alpha-1-antitrypsin deficiency

2.Viral Hepatitis

3.Autoimmune Hepatitis

4.Alcohol/Drugs

6.Hepatocellular carcinoma

325
Q

What level of ALT would indicate a viral cause of Liver disease?

A

> 1000

326
Q

What does Obstructive /Cholestatic mean?

A

1.Biliary disease
-Gallstones
-Pancreatic Cancer
-Cholangiocarcinoma

2.Autoimmune
-PBC
-PSC

3.Drugs

327
Q

What 4 drugs are known for causing obstructive jaundice (Cholestasis)?

A

-Flucloxacillin
-Co-amoxiclav
-Sulphonylureas
-Oral Contraceptive Pill

328
Q

What drug can cause Fibrosis of the Liver?

A

Methotrexate

329
Q

What drugs can cause Hepatitis?

A

-Statins
-TB drugs (Rifampicin, Isoniazid)

330
Q

What from bloods and LFT would indicate Alcoholic Hepatitis?

A

HIGH MCV and GGT

331
Q

What is the management for Alcoholic Hepatitis?

A

1.Alcohol cessation
2.Vit B1 replacement (Pabrinex IV)
–> Switch to Thiamine

332
Q

What is a key complication of Alcoholic Hepatitis that needs to be avoided using B1 supplementation?

A

Wernicke’s Encephalopathy

333
Q

What B1 supplementation is used for Alcoholic Hepatitis?

A

-Pabrinex (IV)
-Thiamine

334
Q

What are the symptoms of Alcohol withdrawal?

A

-Coarse tremors
-Tachycardia
-Hypotension
-Confusion
-Occasional Hallucinations
-Seizures

335
Q

What is the treatment for Alcohol withdrawal?

A

Benzodiazepines (Diazepam)

+IV Thiamine (prevent Wernicke’s Encephalopathy)

336
Q

If someone comes in confused and amnesic, what should immediately be given to prevent Encephalopathies?

A

IV Thiamine

337
Q

List the clinical signs of Liver Cirrhosis.

A

-Palmar Erythema
-Leuconychia
-Dupuytren’s contracture
-Jaundice
-Xanthelasma
-Parotid enlargement
-Spider Naevi
-Hair loss
-Caput Medusae
-Striae
-Hepatosplenomegaly
-Ascites

338
Q

What does Leuconychia indicate?

A

Hypoalbuminaemia

339
Q

What is the gold standard for diagnosing Cirrhosis of the Liver?

A

Liver Biopsy (histology)
=Fibrotic streaks and formation of cirrhotic nodules

340
Q

What is the management for Oesophageal Varices Haemorrhage?

A

-Aggressive IV (wide-bore canula) fluid rescus: Crystalloid

-TERLIPRESSIN
-Prophylactic antibiotics

-Urgent GI endoscopy
=Band Litigation

341
Q

What procedure may be done in SEVERE Oesophageal Varices?

A

Temporary Balloon Tamponade
(Sengstaken-Blakemore tube)

342
Q

A patient has Ascites. What would you advise them?

A

Salt restriction

343
Q

What is the treatment for Ascites?

A

Spironalctone
+Loop diuretic (furosemide)

344
Q

A patient presents with sudden onset of feeling unwell, feverish and severe abdominal pain. What could this be and what should be done?

A

Spontaneous Bacterial Peritonitis (SBP) due to E.coli

=Ascitic tap is diagnostic

345
Q

What results would you expect to diagnose Spontaneous Bacterial Peritonitis (SBP)?

A

Ascitic tap:
-CLOUDY and maybe blood stained
-Fluid microscopy: Polymorph / Neutrophil > 250 x10^6 / L

346
Q

What is the treatment of Spontaneous Bacterial Peritonitis (SBP)?

A

IV Broad spectrum antibiotics
+Oral Ciprofloxacin (prophylaxsis for patients with protein < 15g/L)

347
Q

What protein level would require additional propylaxsis in Spontaneous Bacterial Peritonitis (SBP)?

A

<15g/L
=Oral Ciprofloxacin

348
Q
A
349
Q

What are the typical signs and symptoms of a patient with Cholera?

A

-Severe Diarrhoea
-Dehydration
-Vomiting
-Abdominal pain

350
Q

What are the typical signs and symptoms of a patient with Tetanus?

A

-Muscle Spasm
-Fever
-Lockjaw
-Dysphagia

Way to remember:
TetANUS
My Farts Linger Daily

351
Q

What are the typical signs and symptoms of a patient with Typhoid?

A

-Fever
-Headache
-Abdominal pain
-Constipation
-Rash

352
Q

What are the typical signs and symptoms of a patient with TB ?

A

-Chest pain
-Weight loss
-Loss of appetite
-Night sweats
-Haemoptysis

353
Q

What is the incubation period for Salmonella?

A

6hrs-6months

354
Q

What causes the classical symptoms of an acute infection? i.e Fever, Malaise, Aches, Pains and Nausea?

A

The body produces cytokines such as Interferon which causes the global effects.

355
Q

What is Kernicterus?

A

When a baby with Jaundice gets seizures and muscle spasms due to brain damage from the bilirubin crossing the BBB.

356
Q

What is Gilbert’s syndrome?

A

It is a hereditary condition which causes Hyperbilruinaemia due to a Glucuronyl Transferase Definciency and therefore Bilirubin conjugation is slower and therefore less is excreted.

357
Q

How are patients with Gilbert’s Syndrome affected?

A

Asymptomatic with normal bilirubin levels however they can become easily and quickly jaundiced when physically stressed.

358
Q

What gene is affected in Gilbert’s syndrome?

A

UGT1A1

359
Q

How is neonatal jaundice treated?

A

Phototherapy

360
Q

How does carcinoma of the pancreas cause jaundice?

A

Enlargement of the pancreas causes the common bile duct to compress leading to jaundice.

361
Q

How is carcinoma of the head of the pancreas treated?

A

Pancreatoduodenectomy by Whipple resection (removal of the head)

362
Q

How does gallstones (aka Cholethiasis) cause jaundice?

A

Causes obstruction of the biliary system resulting in biliary colic and jaundice.

363
Q

How does Malaria cause jaundice?

A

P.falciparum parasite causes intravascular haemolysis which causes and increase in Bilirubin and therefore Jaundice.

364
Q

How are gallstones obstructing bile ducts treated?

A

Inserting a stent using ERCP or Laparoscopic Cholecystectomy

365
Q

How is Malaria treated?

A

Schizonticides
=type of chemotherapy that kills the parasite in the blood

366
Q

What is the meaning of febrile?

A

Fever

367
Q

What is the meaning of Icteric?

A

Jaundice

368
Q

What are the 3 main causes of Chronic Liver Disease?

A

-Hepatitis
-Haemochromatosis
-Non Alcoholic Fatty Liver Disease

369
Q

What are the causes Abdominal Distension?

A

6Fs- Fat, Fluid, Flatus (gas), Faeces, Fetus, Fuminant mass (a smelly mass)

370
Q

What are Caput Medusae?

A

Engorged paraumbilical veins

371
Q

What is associated with Caput Medusae?

A

Portal Hypertension caused by Liver Cirrhosis

372
Q

What are the causes of Striae (stretch marks)?

A

Ascites, intrabdominal malignancy, cushing’s syndrome, obesity and pregnancy

373
Q

What is Cullen’s sign?

A

Bruising of tissue surrounding the umbilicus

374
Q

What is Cullen’s sign associated with?

A

Haemorrhagic Pancreatitis (late sign)

375
Q

What is Grey-Turner’s sign?

A

Bruising in the flanks

376
Q

What is Grey-Turner’s sign associated with?

A

Haemorrhagic Pancreatitis

377
Q

What does a raised AST and a normal ALT indicate?

A

AST AND ALT raised would indicate damage to the hepatocytes (liver). But if only AST is raised, that would instead point to muscle damage.

378
Q

What does an elevated T.Bilirubin indicate?

A

Bile duct / Liver issues, or Haemolytic Anaemia

379
Q

How would you treat a patient with Diarrhoea?

A

-Cessation of eating
-IV rehydration with H2O, NaCl and Sucrose to decrease the gut motility

380
Q

What tests are used for diagnosing diabetes?

A

-Urinary glucose
-Fasting blood glucose
-Fasting plasma insulin
-Glucose tolerance test

381
Q

What result would you expect from a Glucose Tolerance test from a Diabetic patient?

A

Delayed decrease of blood glucose after an oral bolus.

382
Q

What does Cachexia mean?

A

Loss of body mass that cannot be reversed nutritionally e.g Cancer, Aids, Coeliac disease, COPD, Congestive heart failure, TB

383
Q

What does a Hypermetabolic state mean?

A

Elevated levels of cytokines which promote protein breakdown e.g Burns, Trauma, Sepsis

384
Q

What does a positive nitrogen balance mean and when do you get it?

A

When there is an increased demand for protein e.g growth, pregnancy, recovery from illness/trauma

385
Q

What are Peyer’s patches and where are they located?

A

They are numerous lymphoid follicles located in the Submucosa of the ileum.

386
Q

How do Gallstones (Choleithiasis) occur?

A

Gallstones form when bile stored in the gallbladder hardens into stone-like material. This is caused usually by too much cholesterol but can also be due to high bile salts, or bilirubin (bile pigment).

387
Q

What is Steatosis?

A

Fatty change within the liver (accumulation of fatty droplets within the liver)
=Reversible cell injury

Note: You will see this in Non-Alcoholic Liver Disease

388
Q

What is Steatohepatitis?

A

-Accumulation of fat with accompanying inflammatory changes in the liver.
-Low grade chronic inflammation OR
-Bouts of hepatitis (mainly patients with alcohol abuse/addiction)
-Leads to fibrosis

389
Q

What causes steatohepatitis?

A

-High association with ALCOHOL
But also:
-Non-Alcoholic Fatty Liver Disease
-Medications/drugs

390
Q

How may Steatohepatitis affect alcohol abusers differently?

A

Instead of chronic inflammation can manifest as bouts of hepatitis.

391
Q

What does a FibroScan do?

A

Ultrasound probe used to measure :
-the stiffness of the liver (Elastography) as a marker for Fibrosis.
-the degree of fatty change (Steatosis) which is expressed as a CAP score

392
Q

How are the results of steatosis from a FibroScan expressed?

A

As a CAP score.

393
Q

What does Decompensated Liver Disease mean?

A

Acute deterioration in liver function in a patient with cirrhosis

394
Q

What are the characteristics of a patient with acute liver cirrhosis?

A

-Jaundice
-Coagulopathy = impaired synthesis of blood clotting factors
-Encephalopathy =due to hyperammonaemia
-Ascites = impaired albumin synthesis and portal hypertension
-Splenomegaly = portal hypertension
-GI bleeding = Oesophaegal varices

395
Q

What are the clinical signs of a patient with Chronic Liver Disease?

A

-Caput Medusa =Distended epigastric veins around umbilicus
-Splenomegaly = suggests portal hypertension
-Ascites = low albumin and increased portal hypertension
-Leukonychia = white fingernails
-Flapping tremor of outstretched hands (late sign)

396
Q

What does Leukonychia mean?

A

White finger nails

397
Q

What viruses can affect the Liver that are not Hepatotropic viruses (liver specific)?

A

-Herpes Simplex
-Epstein Barr Virus

398
Q

What is the mode of transmission for Hepatitis A?

A

Faecal - Oral

399
Q

How does HepA damage the liver?

A

Immune response to the virus does the actual damaging.

400
Q

Is Hep A acute or chronic?

A

Acute

401
Q

What is the incubation period for HepA?

A

2-6 weeks

402
Q

What does fulminant mean?

A

Severe and sudden onset

403
Q

What is the mode of transmission for Hepatitis B?

A

Blood, Sexual transmission

404
Q

Which Hepatitis viruses can have an asymptomatic carrier state?

A

Hep B

405
Q

What are the serious potential progressions of HepB?

A

5% with chronic Hepatitis lead to cirrhosis and then hepatocellular carcinoma.

406
Q

What is the mode of transmission for Hepatitis C?

A

Blood, contaminations (IV drug abusers, tattoos, haemophiliacs as a result of blood product contamination).

407
Q

Name examples of Autoimmune Liver Disease.

A

-Chronic Hepatitis
-Primary Biliary Cirrhosis (Cholangiopathy)
-Primary Sclerosing Cholangitis

408
Q

What is targeted and affected in Primary Biliary Cirrhosis?

A

Intrahepatic bile ducts

409
Q

What is targeted and affected in Primary Sclerosing Cholangitis?

A

Extrahepatic and Intrahepatic bile ducts

410
Q

What blood results would you expect from a patient with Autoimmune Hepatitis?

A

-Elevated serum IgG
-Positive autoantibodies (Anti-smooth muscle)
-No evidence of viral infection

411
Q

What other autoimmune disorders is Autoimmune Hepatitis associated with?

A

-Rheumatoid Arthiritis
-Thyroiditis
-Sjorgren’s syndrome
-Ulcerative colitis

412
Q

What age and gender are usually patients with Primary Biliary Cirrhosis?

A

(90%) Female
-Around 50yrs

413
Q

What other disease(s) is Primary Biliary Cirrhosis associated with?

A

-Sjogren’s syndrome
-Scleroderma
-Thyroid disease

414
Q

What antibody in particular would you expect to see in a patient’s blood test with Primary Biliary Cirrhosis?

A

Positive anti-mitochondrial autoantibodies

wham BAM I am the antibody
BAM:
(Primary)BILIARY(Cirrhosis)
Anti-Mitochondrial

415
Q

What are the key diagnostic tools for Primary Sclerosing Cholangitis?

A

MRI or ERCP which shows the chronic

416
Q

What other disease is Primary Sclerosing Cholangitis associated with?

A

Chronic IBD and Autoimmune Pancreastitis

417
Q

When is the common onset and what gene causes Haemochromatosis?

A

-Adult onset
-HFE

418
Q

Where do you find Peyer’s patches?

A

Throughout the GI tract but the majority of them are in the Ileum.

419
Q

What is a granuloma?

A

Tiny clusters of white blood cells (histiocytes - antigen presenting cells) due to inflammation or irritation. Instead of being phagocytotic, secretes cytokine that recruits more macrophages.
Note: It is not a cancer sign

420
Q

What are the histological findings of a patient with Chron’s Disease?

A

-Transmural inflammation = throughout
-breakdown of mucosa
-damage and inflammation goes into submucosa, muscularis externa and adventitia
-breakdown/ulceration of the epithelial layer
-muscularis externa becomes expanded and fibrotic

421
Q

What are the histological findings of a patient with Ulcerative Colitis ?

A

Breakdown of just mucosa and submucosa
-Lots of inflammatory cells in the submucosa
-Large blood vessels filled with blood in the mucosa

422
Q

What bacterias are possible to infect the biliary tree?

A

-Enterococcus species
-Enterobacteriaceae e.g E.coli, Salmonella (food poisening), Salmonella typhi (typhoid fever)

423
Q

What does Cholecystitis mean?

A

Inflammation of the gall bladder.

424
Q

What does Cholangitis mean?

A

Inflammation of the biliary tract.

425
Q

What are the characteristic symptoms of a biliary infection?

A

-Pain localising to right upper quadrant of abdomen
-Severe will have pain radiating to back
-Can also refer to shoulder tip on the right.
-Nausea
-Vomitting
-Fever
-Abdominal tenderness
-Can also present with sepsis

426
Q

What findings on abdominal examination would you find for a patient with a Biliary infection and why?

A

If the Biliary infection causes peritonitis:
-Abdominal tenderness
-Reflex guarding
-Rebound tenderness
-Muphy’s sign

427
Q

What is Murphy’s sign and what could it indicate?

A

When the examiner places their hand along the right costal margin, the patient cannot breath in comfortably.

-Can indicate a biliary infection (Acute Cholecystitis)

428
Q

If there are signs of sepsis in addition to a biliary tract infection, what antibodies should be given?

A

-Broad spectrum antibiotics : Beta Lactam / Beta-lactamase inhibitor
=Co-amoxiclav and Clavulanic acid

429
Q

Name a Beta Lactam antibody.

A

Co-amoxiclav

430
Q

Name a Beta-lactamase inhibitor .

A

Clavulanic Acid (aka Amoxicillin)

431
Q

What is an abscess?

A

Destruction of normal tissue due to infection and replacement of normal structure with pus and necrotic tissue.

432
Q

Why can’t antibiotics treat an abscess?

A

Due to their low pH, antibiotics can’t work till the pus has been drained.

433
Q

Which other parts of the body can spread their infection to the liver to create an abscess?

A

Appendix, Peritoneum, Colon or Gallbladder can spread to the liver via portal veins

434
Q

What is the treatment for an amoebic infection?

e.g Amoebic Dysentery

A

Metronidazole

435
Q

What type of bacteria is Leptospirosis caused by?

A

Leptospira interrogens
=Spirochetes spiral organisms

436
Q

What are the triad of symptoms for Leptospirosis?

A

Jaundice
Renal failure
Thrombocytopenia (deficiency of platelets in the blood. This causes bleeding into the tissues, bruising, and slow blood clotting after injury).

437
Q

What is the mode of transmission for Leptospirosis and who is mainly affected?

A

Rat urine contamination
-Sewage workers and Triathletes (swimmers)

438
Q

What is the incubation period for Leptospirosis?

A

1-2 weeks

439
Q

What is the prognosis for Leptospirosis?

A

90% resolve naturally after flu like symptoms.
- 5-10% have complications called Weil’s disease: Hepatitis, Jaundice, Haemorrhage and Meningitis

440
Q

What is Weil’s disease?

A

When a patient with Leptospirosis infection have complications such as Hepatitis.

441
Q

How to treat Weil’s disease?

A

Doxycycline

442
Q

How to diagnose Weil’s disease?

A

Serology

(=checking for antibodies in the blood)

443
Q

What blood markers would you expect from a patient with Hep A?

A

IgM

444
Q

What blood markers would you expect from a patient with Hep B?

A

Active / Chronic Infection:
-HBsAg
-HBeAg
note: E antigen indicates infectivity
Recent/Previous Infection :
-HB core Ab

Achieved immunity (via previous or vaccination):
-HB surface Ab

Viral load:
HB DNA PCR

445
Q

A patient has their blood test back with HBsAb present. What does that mean?

A

Past infection of Hep B and therefore have immunity

446
Q

What does the E antigen mean in patients with HepB?

A

Measure of infectivity

447
Q

How to treat Hep C?

A

Sofobuvir

448
Q

How does Viral Hepatitis affect ALP, AST and ALT?

A

ALP decreases
AST and ALT increase

449
Q

How do Antacids work?

A

They are weak alkalis that neutralise acid in the stomach and stimulates mucosal repair through Prostglandin release.

450
Q

What drug do Antacids negatively interact with?

A

Digoxin

(treat heart conditions)

451
Q

How do PPIs (e.g Omeprazole) work?

A

Inhibits protein pumps on parietal cells to stop H+ release in response to food.

452
Q

Why can’t you take Omeprazole when on Warafin?

A

Delays the elimination of Warafin

453
Q

When is Omeprazole prescribed?

A

-Reflux
-Duodenal and Gastric ulcers

454
Q

What exacerbates GORD?

A

Calcium channel blockers, Nitrates, Steroids, NSAIDs

455
Q

How can NSAIDs cause a peptic ulcer?

A

They inhibit Prostaglandin which protects the duodenum and stomach from gastric acid and pepsin.

456
Q

How to treat peptic ulcers?

A

H2 receptor antagonists (e.g Cimitidine) (for symptomatic relief) or PPIs

457
Q

What red flags require an urgent upper GI endoscopy?

A

-Chronic bleeding / Fe deficiency (anaemia)
-Weight Loss
-Dysphagia
-Persistent vomiting
-Persistent
-Dyspepsia (esp over 55 yrs)

458
Q

What two classes of drugs can cause constipation?

A

-Opioids e.g tramadol, oxycodone etc
-Anti-muscarinics e.g Atropine, Ipratropium Bromide

459
Q

What is the first line treatment for constipation?

A

-Fybogel (bulk-forming laxative)

460
Q

What is the contraindication for prescribing Fybogel?

A

If the patient is on opiods

461
Q

What should be prescribed for opioid induced constipation?

A

-Osmotic laxatives: Macrogels (Movicol)

-Also give a stimulant laxative:
Bisacodyl

462
Q

What other drug should be added on if a patient not only has constipation but the stool is hard?

A

Osmotic laxative: Movicol

463
Q

What is a bulk laxative?

A

Contains fibre to swell and distend the colon

464
Q

What is a stimulant laxative?

A

Agents that stimulate intestinal mobility

465
Q

What is an osmotic laxative?

A

Increases faecal bulk and moistens faeces by pulling water in

466
Q

What is Ascites?

A

Water distension in the peritoneum in the abdomen

467
Q

How do you treat Ascites?

A

-Spironalctone (correct Na+ inblance)
-Furosemide (to correct water retention)

468
Q

How to you treat Oesophageal Varices?

A

Phytomenadione (Vitamin K)
=stops varice bleeding for 6-8hrs)

469
Q

What organs are in the right hypochondrium region of the abdomen?

A

Liver
Gallbladder
Right Kidney

470
Q

What organs are in the epigastric region of the abdomen?

A

-Stomach
-Liver
-Pancreas
-Duodenum
-Spleen
-Adrenal glands

471
Q

What organs are in the left hypochondrium region of the abdomen?

A

-Stomach
-Left kidney
-Spleen
-Liver (tip)
-Pancreas

472
Q

What organs are in the right lumbar region of the abdomen?

A

-Small intestine
-Ascending colon
-Right kidney

473
Q

What organs are in the umbilical region of the abdomen?

A

Duodenum, Small intestine,
Transverse Colon

474
Q

What organs are in the left lumbar region of the abdomen?

A

Descending colon
Small intestine
Left kidney

475
Q

What organs are in the right iliac region of the abdomen?

A

Appendix
Cecum
Ascending colon
Small intestine

476
Q

What organs are in the suprapubic region of the abdomen?

A

Bladder
Sigmoid Colon
Reproductive organs

477
Q

What organs are in the left iliac region of the abdomen?

A

Sigmoid colon
Descending colon
Small intestine

478
Q

A patient is suffering pain in the right hypochondrium region. What are the possible causes?

A

-Hepatitis
-Heptatic Abscess
-Cholecystitis
-Cholangitis
-Gallstones

479
Q

A patient is suffering pain in the epigastric region. What are the possible causes?

A

-Gastritis
-GORD
-Peptic Ulcer
-Gastric perforation
-Gastroparesis
-Pancreatitis

480
Q

A patient is suffering pain in the left hypochondrium region. What are the possible causes?

A

-Pancreatitis
-Splenic Infarct
-Splenic Rupture
-Splenic Abscess

481
Q

A patient is suffering pain in the right lumbar region. What are the possible causes?

A

-Kidney stones
-Pyelonephritis
-Ulcerative Colitis

482
Q

A patient is suffering pain in the umbilical region. What are the possible causes?

A

GRAM:
-Gastroenteritis
-Rupture Abdominal Aorta Aneurysm
-Acute Small Bowel Obstruction (SBO)
-Mesentery Ischaemia

483
Q

A patient is suffering pain in the left lumbar region. What are the possible causes?

A

-Kidney stones
-Pyelonephritis
-Colitis

484
Q

A patient is suffering pain in the right iliac fossa region. What are the possible causes?

A

-Appendicitis
-Ulcerative Colitis
-Ovarian Torsion
-Tubo-ovarian abscess (TOA)
-Ovarian cyst

485
Q

A patient is suffering pain in the suprapubic region. What are the possible causes?

A

-Cystitis (inflammation of bladder due to infection)
-Pelvic Inflammatory Disease
-Sexually Transmission Infection (STIs)
-Ectopic Pregnancy

486
Q

A patient is suffering pain in the left iliac fossa region. What are the possible causes?

A

-Colitis
-Diverticulitis
-Ovarian Torsion
-Tubo-Ovarian Abscess (TOA)
-Ovarian Cyst

487
Q

At what point does the Abdominal aorta enter the abdominal cavity and divide?

A

T12

488
Q

At what point does the abdominal aorta terminate?

-Mention bony landmark as well as landmark structures.

A

At the common iliac arteries at L4.

489
Q

What are the 3 branches of the abdominal aorta when it divides in the abdomen?

A

1.Coeliac trunk
2.Superior mesentery
3.Inferior mesentery

490
Q

What does the coeliac trunk divide into?

A

1.Left gastric
2.Splenic
3.Common Hepatic

491
Q

Is the stomach retroperitoneal or intraperitoneal?

A

Intraperitoneal

492
Q

What does the common hepatic artery divide into?

A

1.Gastroduodena2.Right Gastric
3.Right Gastro-omental

493
Q

What is the difference between mesentery and omenta?

A

Mesentary is connective tissue with arteries etc, while omenta is just CT to attach organs to the abdominal wall

494
Q

What are the 2 HIV tests?

A

-HIV 1 & 2 Antibody test
-HIV p24 Antigen test

495
Q

When can you test for HIV 1&2 antibodies?

A

3-12 weeks after exposure

496
Q

Where do you usually see HIV 1 infections in the world?

A

USA

497
Q

Where do you usually see HIV 2 infections in the world?

A

Africa

498
Q

When can you do a HIV p24 test?

A

In the first few weeks after exposure

499
Q

What is the HIV p24 test?

A

Present in acute HIV infection in the first weeks of exposure to HIV, the body produces p24 antigen

500
Q

What does Seroconversion mean?

A

Process of developing specific antibodies in the blood as a result of infection / immunisation

501
Q

What is the difference between compensated and decompensated Liver Cirrhosis?

A

Compensated is when the Liver is still working and Decompensated is when the Liver isn’t .

502
Q

What symptoms should you expect from a patient with Compensated Liver Cirrhosis?

A

-Fatigue and weakness
-Poor apetite
-Weight loss
-Nausea / vomiting
-Mild pain / discomfort in upper right quadrant of abdomen
-Fever

Note: you only get the serious signs in decompensated cirrhosis

503
Q

What symptoms should you expect from a patient with Decompensated Liver Cirrhosis?

A

-Jaundice
-Portal Hypertension
(Ascites, Hepatic Encephalopathy, Varices)
-Hepatorenal syndrome

504
Q

What are the 4 most common causes of Liver Cirrhosis?

A

-Alcohol related liver disease
-Non-alcoholic fatty liver disease
-Hep B
-Hep C

505
Q

What can indicate Hepatocellular Carcinoma?

(Note that it won’t always show up)

A

-Raised Serum Alpha Fetoprotein

506
Q

How does Hepatocellular carcinoma develop from Liver Cirrhosis?

A

Cirrhosis has premalignant lesions of dysplastic nodules that can progress to HCC.

507
Q

What are the 3 main Liver autoimmune conditions to know about?

A

-Autoimmune Hepatitis
-Primary Sclerosing Cholangitis
-Primary Biliary Cirrhosis

508
Q

What would you expect from a Liver Profile for a patient with Autoimmune Hepatitis?

A

Hepatic picture:
-High ALT and AST
-Minimal change in ALP

-Autoantibodies

509
Q

What autoantibodies would you expect for type 1 Autoimmune Hepatitis?

A

-Anti-Nuclear Antibodies (ANA)
-Anti-smooth muscle antibodies (Anti​ actin)
-Anti-soluble liver antigen (anti-SLA/LP) ​

510
Q

What is a typical patient of Type 1 Autoimmune Hepatitis?

A

Post-Menopausal women in 40s-50s

511
Q

What autoantibodies would you expect for type 2 Autoimmune Hepatitis?

A

-Anti-liver kidney microsomes 1 (anti-​LMK1)
-Anti-liver cytosol antigen type 1 (anti-​ LC1)

                                                 ​
512
Q

What would you expect from a Liver Biopsy for Autoimmune Hepatitis?

A

Interface Hepatitis = Death of hepatocytes at the interface of parenchyma and the connective tissue of the portal zone, accompanied by a variable degree of inflammation and fibrosis.​

​

513
Q

What treatments would be offered to a patient with Autoimmune Hepatitis?

A

-High dose steroids -Prednisolone
-Immunosuppressants -Azatioprine

514
Q

What is Primary Sclerosing Cholangitis?

A

Intrahepatic and Extrahepatic Bile ducts become inflamed and damaged developing strictures that obstruct bile flow out of the liver and into the intestines. Chronic obstruction leads to hepatitis , fibrosis and cirrhosis.

515
Q

What does Sclerosis mean?

A

Stiffening and hardening of bile

516
Q

What does Cholangitis mean?

A

Inflammation of bile ducts

517
Q

What is Primary Sclerosing Cholangitis highly related to?

A

Ulcerative Colitis
(70% of patients have both)

518
Q

What is a typical patient with Primary Sclerosing Cholangitis?

A

Male, 30-40s (with Ulcerative Colitis)

519
Q

What is the clinical presentation of a patient with Primary Sclerosing Cholangitis?

A

-Pruritus ​

-Jaundice​

-Right Upper Quadrant pain (Right Hypochondrium/Epigastric region)​

-Hepatomegaly​

-Splenomegaly ​

520
Q

What investigations should be done for a suspected Primary Sclerosing Cholangitis patient?

A

-Liver profile
-Magnetic Resonance Cholangiopancreatography (MRCP)
-Colonoscopy (check for ulcerative colitis)

521
Q

What liver profile results would you expect from a patient with Primary Sclerosing Cholangitis?

A

Obstructive picture:
-High ALP
-High bilirubin (later in disease)

522
Q

What does an obstructive picture mean with a liver profile?

A

High ALP (and high bilirubin later in disease)

523
Q

What would you see in an MRCP for a patient with Primary Sclerosing Cholangitis?

A

Bile duct strictures

524
Q

What treatments would be offered for a patient with Primary Sclerosing Cholangitis?

A

-No cure
-ERCP for dominant strictures to insert a stent
-Colestryamine for Pruritus

525
Q

What are possible complications of Primary Sclerosing Cholangitis?

A

Colorectal cancer (in patient with UC as well)​

Cholangiocarcinoma develops in 10-20% of cases​

Fat soluble vitamin deficiencies (Vit A,D,

526
Q

What is Primary Biliary Cholangitis/Cirrhosis ​?

A

Intrahepatic ducts are attacked by immune system causing inflammation and damage to the epithelial cells of the bile ducts leading to obstruction of bile flow and therefore Cholestasis (reduced bile flow). This can lead to liver fibsosis, cirrhosis and failure.​

527
Q

What is a typical patient with Primary Biliary Cholangitis/Cirrhosis ​?

A

Caucasian, Women, 40-60yrs

528
Q

Describe a clinical presentation of a patient with Primary Biliary Cholangitis/Cirrhosis ​?

A

-Pruritus ​

-Jaundice​

-Abdominal pain​

-Hepatomegaly​

-Pale,greasy stools ​

-Dark urine ​

-Xanthoma (cholesterol deposits)

529
Q

What investigations should be done for a suspect Primary Biliary Cholangitis/Cirrhosis ​?

A

-Liver profile
-Liver Biopsy

530
Q

What would you expect from a Liver profile from a patient with Primary Biliary Cholangitis/Cirrhosis ​?

A

-Obstructive picture:
=High ALP (high bilirubin later in disease)

-Autoantibodies

531
Q

What autoantibodies would you expect in a patient with Primary Biliary Cholangitis/Cirrhosis ​?

A

-Anti-mitochondrial antibodies (AMA) = most specific to PBC patients ​

-Anti-nuclear antibodies

532
Q

What would you expect from a Liver Biopsy from a patient with Primary Biliary Cholangitis/Cirrhosis ​?

A

Granulomas​

Portal based inflammation – portal tracts composed of lymphocytes ​

​

533
Q

What treatments would be offered to patients with Primary Biliary Cholangitis/Cirrhosis ​?

​

A

-Ursodeocycholic acid (protect cholangiocytes from damage)

-Colestryamine (treat Pruritus)

534
Q

What are the possible complications of Primary Biliary Cholangitis/Cirrhosis ​?

A

Liver Cirrhosis​

Hepatocellular Carcinoma ​

Fat soluble vit deficiency (A,D,E and K) ​

Thyroid Disease ​

535
Q

What drugs are contraindicated in hepatic dysfunction?

(remember mneumonic)

A

Alan Calls Dave Avoiding Martin’s Ratty Egotistical Pessimism Very Quietly

Amiodarone
Chlorpromazine
Diclofenac
Anabolic steroids
Methotrexate
Rifampin
Erythromycin
Phenytoin
Valproate
Quinidine

536
Q

What is the treatment for HepB?

A

Usually clears up on its own WITHOUT treatment

537
Q

What blood results would you expect from a patient with Jaundice due to Pre-Hepatic causes?

A

-High T.Bilirubin
-SLIGHT raised AST and ALT

538
Q

What blood results would you expect from a patient with Jaundice due to Intra-Hepatic causes?

A

-ALT and AST raised results will be MUCH higher than ALP and GGT raised results.

539
Q

What blood results would you expect from a patient with Jaundice due to Post-Hepatic causes?

A

-ALP and GGT raised results will be MUCH higher than ALT and AST raised results.

540
Q

What does Vertical transmission of Hep B mean?

A

Vertical transmission of HBV is defined as positivity at 6–12 months of life of the hepatitis B surface antigen (HBsAg) or of HBV-DNA in an infant born to an infected mother

541
Q

What is Acetaminophen?

A

aka Paracetamol
(=non-opiod analgesic)

542
Q

What does high does of acetaminophen do?

A

Liver damage - Medical emergency!

543
Q

What is the treatment for a acetaminophen overdose?

A

IV fluids
Antidotal therapy - N-acetylcysteine (Acetadote, Mucomyst)

544
Q

What factors/illnesses can give you a higher likelihood to get drug-induced hepatitis?

A

-Diabetes
-Pregnancy
-Smoking and Alcohol

545
Q

What is the most common drug responsible for drug induced liver injury in the world?

A

Amoxicillin-Clavulonate

546
Q

What are the drugs to know about that can cause drug induced liver injury.

A

-Diclofenac
-Naproxen
-Amiodarone
-Anabolic steroids
-Methotrexate
-Methyldopa
-Statins
-Erythromycin
-Birth control pills

547
Q

What 2 antibiotics are most implicated in liver damage?

A

Amoxicillin/Clavulanic acid
Flucloxacillin
Erythromycin

548
Q

Where does the gallbladder lie?

A

Anterior to the duodenum and below and behind the liver

549
Q

Where the is most common location of gallstones?

A

Hartmann’s pouch
(the mucosal folds of the neck of the gallbladder)

550
Q

Describe the anatomy of the gall bladder.

A

Fundus - round portion that projects into the interior surface of the liver

Body- largest part of the gallbladder

Neck- where the gallbladder tapers to become continuous with the cystic duct leading into the biliary tree

551
Q

Describe the pathway of bile through the biliary tree.

A

1.Newly synthesised from the liver secreted from hepatocytes and drains from both lobes of liver via CANILICULI, INTRALOBULAR DUCTS and COLLECTING DUCTS into LEFT and RIGHT HEPATIC DUCTS.

2.Those ducts merge to form the COMMON HEPATIC DUCT which runs along the HEPATIC VEIN

3.As the COMMON HEPATIC DUCT descends it merges with the CYSTIC DUCT to form the COMMON BILE DUCT

4.It is then joined by the MAIN PANCREATIC DUCT to form the HEPATOPANCREATIC AMPULLA

5.This empties into the duodenum via the MAJOR DUODENAL PAPILLA

552
Q

What is the sphincter of oddi?

A

The muscular valve of the major duodenal papilla where the bile empties into the duodenum

553
Q

What is Charcot’s Triad?

A

-Upper Quadrant Pain
-Fever
-Jaundice

=Typical of Cholangitis

554
Q

What is the definition of Biliary Colic?

A

-Right upper quadrant pain FOLLOWING A FATTY MEAL
(due to the contraction of the gall bladder)

=Gallstones

555
Q

When would a physician think of Cholangiocarcinoma as a possible diagnosis? What is the red flag symptom / test result?

A

-Painless Jaundice
-Obstructive Liver Profile picture (without pain)

556
Q

What presentation would you usually suspect for a patient with drug induced liver damage?

A

-Abnormal liver profile (usually obstructive)
-Jaundice
-No pain (usually)

557
Q

What is Trimethorprim?

A

Antibiotic usually used to treat UTIs.

558
Q

What is Hepatic Encephalopathy?

A

Brain dysfunction caused by advanced liver failure.

559
Q

What type of tremor would you see in a patient with advanced liver damage?

A

-Liver flap
-Asterixis
-Coarse tremor (very noticable)

560
Q

A patient has suspect Cirrhosis but their ALT is normal. How may this change the diagnosis?

A

It doesn’t! Patients with Cirrhosis can have normal ALT.

561
Q

Name 2 drugs given for treating Diarrhoea?

A

Opioid agonists include
-Loperamide
-Diphenoxylate

562
Q

What drug is Rantidine and what is the most common side effect?

A

H2 antagonist used for GORD
=Decrease of Sex Drive:(

563
Q

Who is a typical patient of Chronic Mesenteric Ischemia?

A

Common in Elderly specifically those predisposed to Atherosclerotic disease
(e.g Diabetics, smokers, hypertensive patients and those with dyslipidemia)

564
Q

What is Chronic Mesenteric Ischaemia?

A

Ischaemia of the mesenteric arteries supplying the intestines
AKA INTESTINAL ANGINA
=general chronic epigastric pain

565
Q

How does Hyponatremia present?

A

Confusion, irritability, weakness and if severe even seizures

566
Q

List a few common causes of Hyponatremia.

A

Renal failure,
Liver failure,
Heart failure,
Addison’s disease
Syndrome of Inappropriate Anti-diuretic Hormone (SIADH)

567
Q

How does Hypermagnesemia present?

A

low blood pressure, neuromuscular depression, respiratory depression, and even CNS depression if severe

568
Q

What causes Hypermagnesemia?

A

Renal failure and excessive intake of antacids.

569
Q

How does Hypocalcemia present?

A

Cramps, spasms, perioral numbness and seizures.

570
Q

List a few common causes of Hypocalcemia.

A

With a low phosphate:
-Acute pancreatitis
-Osteomalacia.
With a high phosphate:
-Hypoparathyroidism
-Chronic kidney disease.

571
Q

What are the common causes of Hyperkalaemia?

A

Chronic kidney disease
-ACE inhibitors
-Potassium-sparing diuretics.

572
Q

What is Zollinger-Ellison syndrome?

A

Excessive levels due to gastrin-secreting tumour. The majority of these tumours are found in the first part of the duodenum, with the second most common location being the pancreas.

573
Q

What other condition is Zollinger-Ellison syndrome associated with?

A

MEN type 1 syndrome

574
Q

How do you diagnose Zollinger-Ellison syndrome?

A

Fasting gastrin levels: the single best screen test
secretin stimulation test

575
Q

What does a positive urea breath test indicate?

A

Presence of H.Pylori which causes Duodenal Ulcers

576
Q

Is H.Pylori:
- Gram negative or positive?
-Oxidase or urease positive?

A

Gram-Negative
Oxidase positive

577
Q

List a few causes of an increased tendency for Thrombosis.

A

-Protein C Deficiency
-Pregnancy
-Hepatocellular Carcinoma

578
Q

What is a Protein C deficiency and how can it affect the Liver?

A

Hereditary thrombosis syndrome whereby the inactivation of clotting factors Va and VIIIa are impaired. As a results patient have an increased risk of developing thrombus, and if this happens in the hepatic veins, Budd-Chiari syndrome results.

579
Q

What is Budd-Chiari syndrome?

A

Disease affecting patients with haematological disease or another procoagulant condition
=THROMBOSIS IN THE HEPATIC VEINS

580
Q

How does Budd-Chiari present?

A

Abdominal pain: sudden onset,
Severe
Ascites → abdominal distension
Tender hepatomegaly

581
Q

What is the first investigation to be done for a suspected Budd-Chiari?

A

Ultrasound with Doppler flow
=No blood flow in the hepatic veins

582
Q

List the causes of Budd-Chiari.

A

Polycythaemia rubra vera
thrombophilia:
Activated protein C resistance,
Antithrombin III deficiency, Protein C & S deficiencies
Pregnancy
Combined oral contraceptive pill: accounts for around 20% of cases

583
Q

20% of Budd-Chiari is due to….

A

Oral contraceptive pill

584
Q

Chron’s is —– mediated.

A

Th1

585
Q

Ulcerative Colitis is —— mediated.

A

Th2

586
Q

What genes are associated with Coeliac Disease?

A

HLA-DQ2 and HLA-DQ8

587
Q

What is Co-danthramer and when is it prescribed (and why)?

A

Laxative for constipation
BUT DUE TO ITS CARCINOGENIC RISKS ONLY GIVEN TO PALLIATIVE PATIENTS WHEN OTHER LAXATIVES HAVEN’T WORKED

588
Q

What are watershed areas and name 2 in the colon?

A

Area where 2 arteries anastamose and supply an area and therefore is at HIGH RISK OF ISCHAEMIA:

1.Splenic flexure (Griffiths point)
2.Rectosigmoid junction (Sudek’s point),

589
Q

What is Ischaemic Colitis?
-Who is affected?
-Where is affected?

A

Ischaemia to blood vessels usually affecting watershed areas of the colon.
=Elderly patients and those with Atrial Fibrillation

590
Q

What is the treatment for Urge Incontinence?

A

First Line
=Oxybutynin, tolterodine (immediate release) or darifenacin

Second line (if first doesn’t work)
=Mirabegron

591
Q

Describe a typical presentation of post-partum psychosis and what should be done?

A

Immediate hospitalisation and anti-psychotic medications (e.g Olanzapine)

592
Q

What is an adnexal mass?

A

Growth that develops around the uterus, usually in your ovaries, fallopian tubes and neighboring connective tissues. Some adnexal tumors are fluid-filled, while others are solid.

593
Q

What is Prolonged Neonatal Jaundice and when does it presents?

A

Idiopathic jaundice caused from BREASTFEEDING which means jaundice isn’t present till 4-7days after birth. This is the cause of jaundice that is prolonged.

594
Q

What are the 3 causes of jaundice in a baby after 24hrs from their birth?

A

Haemolytic disease of the newborn
Infections
G6PD deficiency

595
Q

What are the 3 causes of jaundice in a baby after 24-72hrs from their birth?

A

Physiological
Sepsis
Polycythaemia Vera (PCV)

596
Q

What are the 3 causes of jaundice in a baby after 72hrs from their birth?

A

Extrahepatic biliary atresia
Sepsis
Congenital hypothyroidism
Breastfeeding

597
Q

What is AFP a marker for?

A

Alpha-Fetoprotein
=produced by the Liver so raised level indicates LIVER CANCER or Metastases to liver

598
Q

What is Clostridioides difficile?

A

=Gram positive rod anaerobic bacteria, often encountered in hospital practice. It produces an exotoxin which causes intestinal damage leading to a syndrome called pseudomembranous colitis. C. difficile develops when the normal gut flora are suppressed by broad-spectrum antibiotics.

599
Q

What causes pseudomembranous colitis?

A

C.difficile bacteria:
-In hospital
-PPIs

600
Q

What are the characteristic features of Pseudomembranous Colitis?

A

Diarrhoea
Abdominal pain
Raised white blood cell count (WCC)

601
Q

What are the upper endoscopic findings of Eosinophilic Oesophagitis?

A

Upper endoscopy findings show rings and have linear furrows.

602
Q

What is Eosinophilic Oesophagitis?

A

Allergic inflammation of the oesophagus due to invasion of eosinophils.
Can be due to asthma or eczema or could simply be due to an sensitivity to the ingested food.

603
Q

What group of people are most commonly affected by Eosinophilic Oesophagitis?

A

Males (30-50yrs)

604
Q

What is Metoclopramide and what are the side effects in children / young adults which may mean it should be avoided?

A

=Anti-emetic - for nausea and vomiting

=Oculogyric crisis - a dystonic reaction characterised by a prolonged involuntary upward gaze of the eyes.

605
Q

What is oes Plummer Vinson but you at high risk of?

A

Squamous cell carcinomas of the oesophagus.

606
Q

What is Intussusception?

A

The invagination of one portion of the bowel into the lumen of the adjacent bowel, most commonly around the ileo-caecal region affecting usually infants between 6-18mnths (or toddlers) with boys being twice more likely to have it.

607
Q

What is the presentation of Intussusception?

A

-Intermittent, severe, crampy, progressive abdominal pain
inconsolable crying
During paroxysm the infant will characteristically draw their knees up and turn pale
Vomiting
Bloodstained stool - ‘red-currant jelly’ - is a late sign
Sausage-shaped mass in the right upper quadrant

608
Q

What is the first line treatment for Intussusception?

A

Reduction by air insufflation under radiological control

609
Q

If a kidney stone where to rupture the organ wall, what fluid would leak, into what space would it leak and what structure would it most likely come into contact with?

A

Most commonly by the ureters
=URINE WOULD LEAK

Kidney are RETROPERITONEAL so would contact RETROPERITONEAL structures such as:
Duodenum (2nd, 3rd, 4th parts)
Ascending colon
Descending colon
Pancreas
Kidneys
Ureters
Aorta
Inferior vena cava

610
Q

What are the abdominal retroperitoneal structures?

A

Duodenum (2nd, 3rd, 4th parts)
Ascending colon
Descending colon
Pancreas
Kidneys
Ureters
Aorta
Inferior vena cava

611
Q

What are the abdominal intraperitoneal structures?

A

Stomach
Duodenum (1st part)
Jejunum
Ileum
Transverse colon
Sigmoid colon

612
Q

What is a key side effect of long term use of steroids that is especially riskier if they have has alcohol / substance abuse in the past?

A

Mania (psychiatric issues such as depression)

Clinical scenarios by CBL (8 decks)

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