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Year 3 Medicine > GI > Flashcards

GI Flashcards

1
Q

Define Crohns

A

Chronic inflammatory disease characterised by transmural inflammation anywhere from mouth to anus
Characterised by skip lesions and non caseating granulomas

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2
Q

What are three microscopic features of Crohns?

A

Fissuring Ulcers
Lymphoid and Neutrophil aggregates
Non caseating granulomas

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3
Q

Give 3 presentations of Crohns

A

Diarrhoea
Abdominal Pain
Weight Loss

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4
Q

What are three extra-enteral manifestations of Crohns?

A

Skin - Erythema Nodosum
Eyes - Episcleritis/Iritis/Conjunctivitis
Joint - Ankylosing Spondylitis

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5
Q

Define UC

A

Chronic inflammation of mucosa and submucosa affecting the rectum and extending proximally
Continuous in nature

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6
Q

What are three microscopic features of UC?

A

Crypt Abscesses
Pseudopolyps
Hyperaemic Mucosa

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7
Q

Give three presentations of UC

A

Episodic Diarrhoea
Blood and Mucous
Cramping

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8
Q

What is faecal calprotectin and when is it raised?

A

Indicates neutrophil migration into intestinal mucosa (higher the level, the more inflammation)

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9
Q

What would you see on an Abdo Xray of IBD?

A

Mucosal Thickening
?Proximal Constipation
?Toxic Megacolon

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10
Q

What are the endoscopy options for IBD?

A

Colonoscopy - proximal large bowel disease
Flexible Sigmoidoscopy - safest if diarrhoea is bloody
Capsule Endoscopy - Small Bowel

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11
Q

When would you do an MRI in IBD?

A

For Small Bowel Crohns

For Peri-Anal disease in Crohns

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12
Q

What is the induction management for Crohns?

A

Mild - Prednisolone Orally 40mg for 1/52

Mod/Severe - IV Hydrocortisone and VTE Prophylaxis

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13
Q

What is the induction management for UC?

A

Mild - Mesalazine and Prednisolone Enemas
Mod - Mesalazine and Oral Prednisolone
Severe - IV Hydrocortisone, Cyclosporine

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14
Q

What is the maintenance therapy for IBD?

A

Step Ups
Steroids
Azathioprine
Infliximab

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15
Q

When is Azathioprine started in IBD?

A

If unresponsive to steroids

If requiring more than two rescue therapies a year

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16
Q

Other than nausea, give two side effects of Azathioprine

A

Pancreatitis

Leucopenia

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17
Q

How does Infliximab work? What do you have to test for prior to prescription?

A

Prevents neutrophil aggregation and granuloma formation

Check for underlying malignancy and TB

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18
Q

Define Coeliac

A

Immune mediated inflammatory systemic disorder provoked by gluten

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19
Q

Describe the pathophysiology of Coeliac disease

A

Associated with HLA DQ2 and HLA DQ8
Lengthening of intestinal crypts
Lymphocytes infiltrate epithelium

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20
Q

Give 5 presentations of Coeliac Disease

A 
Bloating
Diarrhoea
Weight Loss
Steatorrhoea 
Abdo Pain
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21
Q

What blood tests would you carry out for suspected Coeliac disease?

A

Total IgA

tTG-IgA (AKA Tissue Transglutaminase IgA)

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22
Q

What other investigation (not bloods) would you carry out for suspected Coeliac disease

A

OGD and Duodenal Biopsy

Showing villous atrophy and intraepithelial lymphocytosis

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23
Q

Give four complications of Coeliac Disease

A

Small Bowel Lymphoma
Small Bowel Cancer
Osteoporosis
Neuropathy

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24
Q

What are the 5 Key Questions to ask a patient presenting with Dysphagia?

A

1) Was there difficulty swallowing both solids and liquids from the start?
2) Is it difficult to initiate swallowing?
3) Is swallowing painful?
4) Is dysphagia intermittent or getting worse?
5) Does neck bulge and gargle on drinking?

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25
Q

Give two physical causes of Oesophageal Dysphagia

A

Tumour

Stricture

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26
Q

Give two neuromuscular causes of Oesophageal Dysphagia

A

Achalasia

Presbyoesophagus

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27
Q

How would you investigate Physical causes vs Neuromuscular?

A

Physical with OGD

Neuromuscular with Barium Swallow

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28
Q

What is Oropharyngeal Dysphagia?

A

Difficulty getting food to leave the mouth due to lack of coordination

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29
Q

Give a brief outlne of the four stages of Hepatic Encephalopathy

A

1 - Poor Memory and Sleep
2 - Asterixis, Agitation
3 - Drowsy
4 - Coma

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30
Q

What does a raised ALT indicate vs a raised ALP?

A

ALT - damage to hepatocytes

ALP - damage to bile ducts

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31
Q

What is Gamma GT?

A

An enzyme found in hepatocytes and biliary tract

Needs to be raised alongside ALP (as ALP can also be raised in increased bone turnover)

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32
Q

Name two autoantibodies associated with Primary Biliary Cirrhosis

A

AMA (Antimitochondrial Antibodies)

SMA (Smooth Muscle Antibodies)

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33
Q

Name 6 components of a liver screen

A 
Hepatitis Serology
Iron Studies (Transferrin and Ferritin)
Autoantibodies
Immunoglobulins
Ceruloplasmin
Alpha - 1 Antitrypsin
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34
Q

What are the three most common causes of Chronic Liver Disease?

A

Alcoholic Liver Disease
Non Alcoholic Steatohepatitis (NASH)
Hep B and C

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35
Q

What is PBC? Give three feature?

A

Autoimmune granulomatous inflammation of intra and extrahepatic bile ducts
Associated with AMA antibody
More common in Women
Asymptomatic raised ALP

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36
Q

What is autoimmune hepatitis?

A

Autoantibodies against hepatocyte surface antigens

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37
Q

Describe the presentation of autoimmune hepatitis

A

Acute hepatitis

Jaundice

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38
Q

What is PSC? How do patients present?

A

Primary Sclerosis Cholangitis is progressive cholestasis with bile duct inflammation and strictures
Presents as pruritus with or without fatigue

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39
Q

What is the risk if a patient has IBD and PSC?

A

Increased risk of colorectal malignancy

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40
Q

What is Haemachromatosis?

A

Autosomal Recessive (HFE gene) of increased iron absorption leading to deposition in skin/joints/organs

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41
Q

Why do women with Haemachromatosis present later than men?

A

Menstrual blood loss is protective

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42
Q

What are the early and late presentations of HH?

A

Early - may be asymptomatic or have lethargy/anthralgia

Late - Slate grey pigmentation, Chronic Liver Disease, Dilated Cardiomyopathy

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43
Q

What would the serology of HH show?

A

Raised LFTs
Raised Transferrin Saturation
Raised Ferritin

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44
Q

How would you manage HH?

A

Therapeutic Venesection
Avoid alcohol
Avoid uncooked seafood (listeria thrives on high iron)

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45
Q

What is WIlson’s Disease?

A

Autosomal recessive disorder of copper excretion with deposition in liver and CNS

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46
Q

Give 4 presentations of Wilson’s Disease

A

CNS Signs (Dysarthria, Dysphagia)
Slow Cognition
Decreased Libido
Kayser Fleischer Ring

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47
Q

What would the serology of Wilson’s Disease show?

A

Raised LFTs
Low Serum Copper
Low Serum Ceruloplasmin
(HIGH URINARY COPPER)

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48
Q

Define Cirrhosis

A

End pathology of Chronic Liver Disease implying irreversible liver damage

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49
Q

Give three histological features of Cirrhosis

A

Loss of Architecture
Fibrosis
Nodular Regeneration

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50
Q

Give 5 signs of Cirrhosis OE

A 
Clubbing
Palmar Erythema
Dupuytren's Contracture
Spider Naevi
Gynaecomastia
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51
Q

Name 3 features of Liver Failure

A

Coagulopathy (synthetic failure)
Encephalopathy (PADC)
Ascites

52
Q

What is the risk of Ascites?

A

Spontaneous Bacterial Peritonitis

53
Q

Apart from Liver Failure, give two complications of Cirrhosis?

A

Portal Hypertension

Hepatocellular Carcinoma

54
Q

What drug would you give for hepatic pruritus?

A

Colestyramine

55
Q

What medical management would you give for Hepatic Encephalopathy? How do they work?

A

Lactulose - decreases ammonia reabsorption

Rifaximin - eliminates ammonia producing bacteria

56
Q

What medical management would you give for Ascites?

A

Fluid restriction and spironolactone

57
Q

What is the difference between intentional weight loss and weight loss from illness?

A

Weight loss whilst unwell will be from muscle not fat

58
Q

What is the MUST score?

A

Malnutrition Universal Screening Tool

Identifies adults who are malnourished or at risk of malnourishment

59
Q

What are the five stages of MUST screening?

A

1) BMI
2) %unplanned weight loss scored via table
3) Establish acute disease effects and score
4) Add 1,2,3 and give an overall score
5) Refer to guidelines

60
Q

What would you do for ‘Low Risk’ patients following MUST screening?

A

Routine clinical care

Repeat screning

61
Q

What would you do for ‘Medium Risk’ patients following MUST screening?

A

Document dietary intake for 3 days
Adequate - continue to repeat screenings
Inadequate - follow local policy

62
Q

What would you do for ‘High Risk’ patients following MUST screening?

A

Refer to dietician or nutritional support team

63
Q

Give three reasons so many patients are malnourished

A

NBM
Increased requirements
Direct effect of treatment (N&V)

64
Q

How can you ensure an NG tube is inserted correctly?

A

Test pH

CXR (especially if on PPIs)

65
Q

What is Polymeric Feeding?

A

Unaltered molecules of carbohydrates/proteins/fats for people who can digest and absorb normally

66
Q

What is Elemental Feeding?

A

Nutritive substances in amino acid and monosaccharide form for patients that require pre-digestion

67
Q

What is the ROCKALL score?

A

Predicts the risk of death and rebleeding from an upper GI bleed
Done pre and post endoscopy

68
Q

Give 5 contributions to the ROCKALL score

A 
Age
Co-Morbidity
Shock
Source of Bleeding
Stigmata of recent bleeding
69
Q

What is the Blatchford Score?

A

Used to predict the need for intervention in a GI bleed (intervention being transfusion or therapeutic endoscopy)

70
Q

Give 5 parameters used in the Blatchford Score

A 
Blood Urea
Systolic BP
Malaena
HR>100
Syncope
71
Q

What is the most common cause of GI bleeds?

A

Peptic Ulcers

72
Q

Give a three step management plan for Variceal Bleeds

A

1) Fluid Rescucitation
2) IV Terlipressin (no IHD) and IV antibiotics
3) Urgent Endoscopy

73
Q

Describe the two endoscopy management options for a Varcieal Bleed

A 
Banding (Mechanical obstruction to flow)
Sengstaken Blakemore (Tube with a single balloon)
74
Q

Describe the TIPSS procedure

A

Transjugular Intrahepatic Portosystemic Shunt

Establishes communication between Hepatic Portal Vein and Hepatic Vein in an attempt to reduce portal hypertension

75
Q

What is Dieulofoys?

A

Rupture of an unusually large arteriole

76
Q

How would you manage a Non Variceal bleed?

A

Most stop on their own
IV fluids, bloods
If continues do radiological embolisation

77
Q

Give two examples of malignant liver tumours

A

Hepatocellular carcinoma

Cholangiocarcinoma

78
Q

Give three examples of benign liver tumours

A

Cysts
Hemiangiomas
Adenomas

79
Q

What is Achalasia?

A

Impaired peristalsis of smooth muscle layer of lower oesophagus causing functional stenosis/stricture

80
Q

Give 5 presenting features of Achalasia

A 
Dysphagia (solid>liquid)
Food Bolus Impaction
Regurgitation
Retrosternal Chest Pain
Heartburn
81
Q

What would a CXR of Achalasia show?

A

Vastly dilated oesophagus behind the heart (bird beak)

82
Q

Manometry is the gold standard investigation for Achalasia. What would you do before and why?

A

Barium Swallow in case of puncturing malignancy

83
Q

What would Manometry of Achalasia show?

A

High cardiac sphincter pressure with incompleterelaxation on swallowing

84
Q

What are the two management options for Achalasia?

A 
Heller Myotomy (dividing the cardiac sphincter)
Pneumatic Dilation (balloon catheter to rupture muscle without breaking mucosa)
85
Q

What is Eosinophiilic Oesophagitis

A

Oesophageal symptoms with infilatration of eosinophils into oesophageal epithelium
Originally a type of GORD unresponsive to PPIs

86
Q

What would you see on a biopsy of Eosinophilic Oesophagitis?

A

More than 15 Eosinophils per field

87
Q

Describe the conservative management of Eosinophilic Oesophagitis

A 
Elemental feeding (amino acid) for 6/52
Exclusion of food groups based on allergy testing
88
Q

Describe the pharmacological management of Eosinophilic Oesophagitis

A

Fluticasone Inhaler (sprayed into mouth and swallowed, no eating/drinking for 30 mins after)

89
Q

What drugs if taken incorrectly may be mistaken for GORD?

A

NSAIDs
Doxycycline
Bisphosphonates

90
Q

Give 3 drugs that are a risk factor for GORD. Why?

A

Anticholinergics
Nitrates
CCBs
Relax cardiac sphincter

91
Q

Give 3 requirements for urgent endoscopy

A

Dysphagia
Over 55 AND Weight Loss AND Another GI Symptom
ALARM symptoms

92
Q

Describe an endoscopic grading method for GORD

A 
Savary Millar Grading
1 - Single/Multiple erosions on a single fold
2 -  Multiple erosions on multiple folds
3 -  Multiple circumferential erosions
4 - Ulcer/Stenosis/Shortening
5 -  Barrett's Epithelium
93
Q

Give two other investigations you could do for GORD

A

Barium Swallow

24h pH monitoring

94
Q

Give 4 pharmacological treatment options for GORD

A

Antacids/Alignates
Lansopazole (30mg OD)
Ranitidine
Metacloperamide (Prokinetic)

95
Q

What is Laproscopic Fundoplication?

A

A surgical technique used to treat disorders such as GORD

Involves wrapping the fundus of the stomach around the lower oesophageal sphincter, enhancing it’s strength

96
Q

What are the two types of Hiatus Hernia?

A

Sliding (80%) - GOJ slides up into chest

Rolling (20%) - GOJ remains in stomach but bulge of stomach herniates either side

97
Q

Give 5 foods rich in Vitamin C

A 
Grapefruit
Oranges
Broccoli
Tomatoes
Cabbage
98
Q

Give 3 physiological uses of Vitamin C

A

Collagen Formation
Fascilitating Iron Absorption
Anti-Oxidant

99
Q

Give 5 signs of Scurvy

A 
Anorexia
Gingivitis
Halitosis
Muscle weakness
Gum bleeding
100
Q

What is Pellagra?

A

Defiency of Niacin (Vitamin B3)

101
Q

Give 3 sources of Niacin

A

Beans
Milk
Converted from Tryptophan in deficient states (this is inhibited by Isoniazid - hence give Pyrazinamide)

102
Q

What is Niacin used for?

A

Precursors for vital metabolic enzymes NAD and NADP

103
Q

What is the triad of Pellagra?

A

Diarrhoea
Dementia
Dermatitis (Casal’s Necklace)

104
Q

How would you diagnose and manage Pellagra?

A

Diagnosed - Low levels of Niacin metabolites

Managed - Nicotinamide

105
Q

What is Beri Beri?

A

Thiamine (Vitamin B1) Deficiency

106
Q

Give 3 risk factors for Beri Beri

A

Alcoholism
Aids
Hyperemesis Gravidarum

107
Q

Describe the two types of Beri Beri

A

Wet - Symptoms of Heart Failure

Dry - Symptoms are Neurological/Muscular

108
Q

How would you manage Beri Beri?

A

Oral Thiamine

Diet - Whole grains, Lean pork, Legumes

109
Q

What is Xeropthalmia?

A

Vitamin A Deficiency

110
Q

What is primary and secondary Xeropthalmia

A

Primary - Poor Diet

Secondary - Propblem with storage/transport of Vitamin A (eg Cystic Fibrosis)

111
Q

Give 3 examples of Vitamin A rich food

A

Liver
Milk
Eggs

112
Q

What is Vitamin A used for

A

Converted to photoreceptor pigment in retina

Regulates gene expression and differentiation

113
Q

Give four presentations of Xeropthalmia

A

Night time blindness
Conjunctival Dryness
Bitots Spots (abnormal squamous cell proliferations)
Skin and hair dryness

114
Q

What are Carcinoid tumours?

A

Originate from Enterochromaffin cells and are able to produce Serotonin
Commonly found in appendix, ileum and rectum

115
Q

What is an Octreoscan?

A

Radioactive scan for carcinoid tumours

116
Q

What pharmacological management would you use for Carcinoid Tumours?

A

Octreotide - Somatostatin analogie that will prevent carcinoid crisis

117
Q

What is the triad of Hepatorenal Syndrome?

A

Cirrhosis
Ascites
Renal Failure

118
Q

What is the pathophysiology of Hepatorenal Syndrome?

A

Portal hypertension reduces portal blood supply, causing blood to pool in splanchnic circulation
As a result you get vasodilation, and reduced BP
RAAS activated resulting in afferent vasoconstriction and AKI

119
Q

What is the diagnostic criteria for Hepatorenal Syndrome?

A

Cirrhosis with ascites
Serum creatinine>1.5mg/dl
Absence of shock/hypovolaemia/nephrotoxins/parenchymal renal disease

120
Q

What’s the difference between Type 1 and Type 2 Hepatorenal Syndrome? How does their management differ?

A

1 - Doubling of serum creatinine in less than two weeks, usually preceded by infection. Managed with Terlipressin and ideally liver transplant.
2 - More steady deterioration. Managed with TIPS

121
Q

Give 2 examples of H1 receptor antagonist anti-emetics

A

Cyclizine

Cinnarizine

122
Q

Give 4 examples of D2 receptor antagonists. Give a use.

A 
Metaclopramide
Domperidone
Prochlorperazine
Haloperidol
Hyperemesis Gravidarum
123
Q

Name a 5HT3 antagonist and its use

A

Ondansetron

PONV

124
Q

Give three differences between Gastric and Duodenal ulcers

A

Pain time after eating (1-2hrs G, 2-4hrs D)
Food aggravates pain (G), Food relieves pain (D)
Vomiting common (G), Vomiting uncommon (D)

125
Q

What is Wernicke- Korsakoff Syndrome?

A

Encephalopathies as a result of Thiamine deficiency (Dry Beri Beri)
Wernickes Encephalopathy- Acute Reversible form (medical emergency)
Korsakoff Syndrome - Chronic and Irreversible form (from untreated Wernickes)

126
Q

What is the triad of Wernicke’s Encephalopathy?

A

Opthalmoplegia, Ataxia, Confusion

127
Q

How does Korsakoff Syndrome present?

A

Targets the Limbic System:
Impaired Memory (anterograde and retrograde)
Confabulation (making up information to replace lost memories)

Year 3 Medicine (15 decks)

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