12 - Gastroenterology Flashcards

1
Q

What are some causes of diarrhea?

A
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2
Q

How do most patients with IBD present initially, and how do you take a history of this presenting system?

A

Change in bowel habit

  • How often and is this different from usual?
  • Has the form changed?
  • Any blood?
  • Tenesmus?
  • Faecal urgency or incontinence?
  • Do they easily flush?
  • Waking in night to defecate?
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3
Q

What are the differences between Crohn’s and UC?

A
  • Crohn’s has perianal disease but UC does not
  • Crohn’s often non-bloody but UC is bloody
  • Crohn’s has skip lesions but UC constant
  • Crohn’s is transmural but UC superficial
  • Crohn’s has granulmoas but UC has crypt abscesses
  • Crohn’s worsened by smoking but UC smoking is protective
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4
Q

If a patient presents with change in bowel habit, what are some investigations you should do and what might they show?

A
  • Blood Tests (FBC, ESR, CRP)
  • Stool Tests (to exclude infective causes)
  • Faecal Calprotectin (not diagnostic of IBD so no point using if there’s blood)
  • AXR
  • Endoscopy
  • CT/MRI
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5
Q

If a patient presents with an IBD flare, you do an AXR and flexi sig, what do they show?

A

AXR: proximal constipation and assess for toxic megacolon

Flexi Sig: inflammation, safer than colonoscopy

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6
Q

What are some of the symptoms and signs of UC?

A

Symptoms:

  • Episodic or chronic diarrhoea
  • Mucus or bloody stools
  • Crampy abdominal pain
  • Tenesmus due to proctitis

Signs: fever and tender distended abdomen if acute, clubbing, oral ulcers, erythema nodosum

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7
Q

How do you assess the severity of UC?

A

Truelove and Witt’s Criteria

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8
Q

What are some of the complications with UC?

A

Acute:

  • Toxic megacolon with risk of perforation
  • VTE
  • Low K+

Chronic:

  • Colon cancer (surveillance colonoscopy with multiple random biopsies)
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9
Q

How is chronic UC managed?

A

Goals are to induce then maintain remission

GIVE BONE PROTECTION AS IBD AND STEROIDS RISK FOR OSTEOPOROSIS

1st Line: Mesalazine (5-ASA) for induction/remission

2nd Line: Azathioprine and Biologics

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10
Q

How is acute UC managed?

(use image)

A

- Prophylactic heparin as high VTE risk

- Steroids (usually IV hydrocortisone but can have oral/rectal) to induce

- Rescue therapy if not responding in 3-5 days is ciclosporin, biologics or surgery (colectomy)

Mesalazine is used for remission maintence and second line for that is azathiporine and biologics
Also Mesalazine is an aminosalicyate so can be used in mild/moderate

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11
Q

What monitoring is needed for acute UC treatments as immunosuppressants are used in the treatment?

A
  • FBC
  • U+Es
  • LFTs
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12
Q

What surgery is done for UC patients?

A

Subtotal colectomy and terminal ileostomy if failure of medical therapy or toxic megacolon

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13
Q

What are some of the signs and symptoms of Crohn’s?

A

Symptoms:

  • Diarrhoea
  • Abdominal pain
  • Weight loss
  • Fatigue, fever, malaise

Signs: bowel ulceration on colonoscopy, perianal abscess, skin tags, fistulas, skin and eye problems

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14
Q

What can exacerbate Crohn’s?

A
  • Smoking
  • NSAIDs
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15
Q

What are some complications with Crohn’s?

A
  • SBO
  • Toxic megacolon
  • Abscess fromation
  • Fistulae e.g entero-enteric, colovesical
  • Colon cancer
  • Malnutrition
  • Perianal disease
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16
Q

What investigations should you do if you suspect Crohn’s?

A

- Bloods: FBC, U+Es, ESR, CRP, B12, Folate, Ferritin

- Stool culture: exclude E.Coli, Shigella, Campylobacter

- Colonoscopy and biopsy

- Capsule endoscopy

- MRI

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17
Q

How is chronic Crohn’s managed?

A
  • Quit smoking and optimise nutrition

- 1st Line: Oral steroids (prednisolone) to induce

- 2nd Line: Azathioprine if relapsing on steroid taper or Biologics like Anti-TNFa

- 3rd Line: Surgery to either resect affected areas, or control perianal disease

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18
Q

How is acute Crohn’s managed?

A
  • IV hydration/eclectrolytes
  • IV hydrocortisone
  • VTE prophylaxis
  • Consider nutritional support
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19
Q

What is the mainstay of treatment for acute IBD?

A
  • Prophylactic IV heparin
  • Steroids
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20
Q

What is the first choice medication for perianal disease or fistulating disease in Crohn’s?

A

Biologics like anti-TNFa then surgery

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21
Q

What are some side effects of Azathioprine and Infliximab used in Crohn’s treatment?

A

Azathioprine (monitor FBC, U+Es, LFTs): abdominal pain, hepatitis, pancreatitis, leucopenia

Infliximab (check CXR and IGRA for TB): lymphoma risk, reactivate TB,

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22
Q

What are some of the side effects of Mesalazine (5ASA)?

A

Decreases risk of colorectal cancer but:

  • diarrhoea
  • headache
  • nausea & rash
  • interstitial nephritis
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23
Q

What is the pathophysiology of coeliac disease?

A

Autoimmune condition where T cells react to the gliadin fraction of gluten and cause villous atrophy in the small bowel and malabsorption

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24
Q

When should you suspect coeliac disease?

A
  • Diarrhoea with weight loss and iron deficiency/B12 anaemia
  • FHx in first degree relative
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25
Q

What are some symptoms of coeliac’s disease?

A
  • Loose stools
  • Stinking stools/Steatorrhea
  • Bloating
  • Wind
  • Weight loss
  • Dermatitis herpetiformis
  • Mouth ulcers
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26
Q

What are some of the complications of Coeliac’s disease if left untreated?

A
  • Small bowel lymphoma
  • GI cancer
  • Osteoporosis
  • Gluten ataxia
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27
Q

How is coeliac disease diagnosed?

A

Diagnostic test:

OGD and duodenal biopsies whilst on gluten-containing diet. Will show villous atropy, intraepithelial lymphocyte infiltration and crypt hyperplasia

Supporting tests:

- IgA Tissue Transglutaminase and Total IgA in case of deficiency (do biopsy if positive serology)

  • Anaemia
  • Low ferritin and B121

MUST CONTINUE EATING NORMAL GLUTEN DIET UNTIL DIAGNOSIS!!!!

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28
Q

How is coeliac’s disease treated?

A

Refer to dietician for lifelong gluten-free diet. Remove:

  • Barley
  • Rye
  • Oats (might be ok)
  • Wheat

Can still eat: potatoes, maize, soya, sugar, rice

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29
Q

What are some important questions to ask in a history if a patient presents with diarrhoea?

A
  • Acute or chronic?
  • Travel?
  • Diet change?
  • Contact with D+V?
  • Bloody? (Campylobacter, Shigella, E Coli, UC, cancer)
  • Mucus? (Polyps, IBS, cancer)
  • Frank pus?
  • Explosive?
  • Steatorrhea?
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30
Q

What are some causes of explosive diarrhoea?

A
  • Rotavirus
  • Giardia
  • Cholera
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31
Q

What are some investigations you should do for diarrhea?

A
  • Examination: assess for dehydration, PR for impacted faeces

- Bloods: FBC, ESR, CRP, coeliac serology, U+Es, TSH

- Stool: culture and faecal elastase

- Lower GI endoscopy: colitis and cancer

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32
Q

How should you manage diarrhea?

A
  • Treat cause
  • Hydration (preferably oral) and Electrolyte replacement
  • Codeine Phosphate or Loperamide (not in colitis as risk of toxic megacolon)
  • Avoid antibiotics unless systemic upset
  • Consider closing ward or informing PHE.
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33
Q

How does C.Diff colitis present and why is it dangerous?

A
  • Diarrhoea wirth systemic upset (raised WCC, CRP)
  • Colitis (yellow plaques)

Can progress to toxic megacolon and then multiorgan failure!!!

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34
Q

How is C.Diff diagnosed?

A
  • Stool test (PCR and ELISA)
  • AXR
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35
Q

How should we treat C.Diff?

A

- Stop causative antibiotic

- Start vancomycine PO for 10 days

  • Prevent spread by isolation, handwashing (not gelling), gloves, cleaning
  • Urgent colectomy if toxic megacolon
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36
Q

What are some red flag symptoms for dyspepsia and reflux? (epigastric pain)

A

ALARMS

  • Anaemia
  • Loss of weight
  • Anorexia
  • Recent onset
  • Melena/Haematemesis
  • Swallowing difficulty
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37
Q

When should you urgently refer to endoscocopy with dysphagia/dyspepsia?

A
  • All patients with dysphagia
  • Patients >55 with ALARM features and dyspepsia
  • Treatment refractory dyspepsia
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38
Q

What are some causes of dyspepsia?

A
  • Duodenal ulcer
  • Gastric ulcer (H.Pylori)
  • Gastritis
  • GORD
  • Malignancy
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39
Q

How is dyspepsia treated (in the absence of red flags)?

A
  • Decrease alcohol and tobacco

- PPI or H2 blockers

- H.Pylori test and eradication therapy if positive

  • Stop any drugs that will precipitate e.g NSAIDs
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40
Q

How is functional dyspepsia treated?

A

NO OBVIOUS CAUSE:

  • PPIs
  • Psychotherapy
  • Amitriptylline
41
Q

What are some causes of dysphagia?

A
42
Q

What are some key questions to ask if a patient is presenting with dysphagia?

A

Need to work out if oesophageal or oro-pharyngeal dysphagia

43
Q

How do you distinguish between oesophageal and oro-pharyngeal dysphagia with your investigations?

A

Oesophageal: Either obstruction or neuromuscular issue. Need OGD first to exclude obstructive cause, then barium swallow or manomoetry to look for neuromuscular issue

Oropharyngeal: Usualy neurological disease like stroke as cannot move bolus to back of mouth. Examine cranial nerves, get speech therapy assessent and videofluroscopy

44
Q

What are some causes of upper GI bleeds?

A
  • Peptic ulcers
  • Varices
  • Mallory Weiss Tear
  • Malignancy
45
Q

What are the different presentations of upper GI bleeds?

A
  • Haematemesis
  • Coffee ground vomiting
  • Melaena
  • Fresh PR bleeding
46
Q

When a patient has an upper GI bleed you must assess a few things after taking a history when first seeing them. What are these?

A

Need to work out if variceal bleed as this is emergency!!!!!!

- Risk factors for bleeding: any known varices, stigmata of chronic liver disease, NSAIDs, anticoagulants, antiplatelets, past GI bleeds

- Is the patient shocked?: clammy, increased cap refill, tachycardic, hypotension

- Rockall Score

47
Q

What are the two assessment scores for GI bleeding and what do they determine?

A

- ROCKALL: Predicts risk of death and rebleeding with upper GI bleed. Pre and post enscopy scores.

- Glasgow Blatchford: Predicts need for intervention with GI bleed with blood transfusion or therapeutic endoscopy. Helps decide whether to admit the patient

48
Q

How do you calculate the Rockall score for upper GI bleeds?

A

Bedside parameters and endoscopy results to predict risk of dying and rebleeding:

  • Age
  • Comorbidity
  • Shock
  • Source of bleeding
  • Stigmata of recent bleeding
49
Q

How do you calculate the Glasgow-Blatchford score for upper GI bleeding?

A

Uses results of basic blood tests before endoscopy to calculate need for admission/intervention:

  • Blood urea
  • Hb
  • Systolic BP
  • Other markers

Score over 6 is 50% chance for needing intervention

50
Q

What initial investigations should you order for a patient with a suspected upper GI bleed?

A

- FBC: check for anaemia and low platelets due to liver disease

- U+Es: will show raised urea

- Clotting: see if any corrections needed

- Group and Save

- Crossmatch: if haemodynamically unstable for blood transfusion

- LFTs

- VBG

51
Q

What is the management for an upper GI bleed due to varices?

A

MEDICAL EMERGENCY

  • Gain IV access with 2 large bore cannulas for bloods and fluids

- NBM

- Fluid resus if haemodynamically unstable whilst waiting crossmatch

- Blood transfusion

- PPI

- Correct any coagulation issues

- IV terlipressin to reduce splanchnic blood flow and I_V broadspectrum abx_

- Urgent endoscopy for banding, Linton tube or TIPSS

52
Q

When should you not give IV terlipressin for variceal bleeding?

A
  • Ischaemic heart disease
  • Peripheral vascular disease
53
Q

What is the management for an upper GI bleed that is not due to varices?

A

- Gain IV access for bloods and fluid resus if haemodynamically unstable. Transfuse if Hb<70 and correct any clotting abnormalities. Give platelets if actively bleeding

- Catheterise and fluid balance

- Endoscopy with adrenaline injections (may need PPI and H.Pylori eradiaction after based on findings/biopsy)

54
Q

What is some prophylaxis for variceal bleeds if a patient is known to have varices?

A

Varices are due to portal hypertension from cirrhosis so lower this pressure:

  • Propanolol (B-blocker)
  • Endoscopic banding
55
Q

What are the different classifications of haemorraghic shock?

A

IMPORTANT

56
Q

After haemostasis has been achieved with an upper GI bleed, what primary prophylaxis should you give to patients to prevent rebleeding?

A
  • PPI
  • Stop NSAIDs
  • Low dose aspirin for secondary prevention of vascular events
  • Discuss whether to continue clopidogrel
57
Q

How do you follow up a patient following a variceal bleed or following haematemesis due to an ulcer?

A
58
Q

When is a patient is sick they experience weight loss due to?

A

Loss of muscle (not fat)

59
Q

What tool is used to assess if a patient is malnourished?

A

MUST

  • Acutely ill and no nutritional intake for >5 days
  • Unplanned weight loss in last 3-6 months
  • BMI
60
Q

How should you manage someone with medium (1) or high (2 or more) risk of malnutrition?

A

Medium: record dietary intake

High: refer to dietician

61
Q

What deficiency syndrome occurs with the following vitamin deficiencies:

  • A
  • B1
  • B2
  • B6
  • B12
  • C
  • D
  • E
  • K
  • Phosphate
A

“BAD NEWS C”:
B12 deficiency - Neurological problems
A - Anemia (B12 + Folate)
D - Deformities (rickets - Vit D)
N - Night blindness (vitamin A)
E - Edema (vitamin K)
W - Weakness (various deficiencies)
S - Scurvy (vitamin C)

62
Q

What is the feeding hierarchy?

A

Should always encoruage oral feeding!

63
Q

What are some ways to support normal oral feeding?

A
  • Stop mealtime interruptions
  • High calorie options encouraged or food fortification
  • Ensure dentures are in
  • Ensure correct cutlery
  • Give assistance with eating
  • Nutritional supplements as suggested by dietician
64
Q

If a patient cannot feed orally despite maximally supporting them or they are not meeting their nutritional requirements with oral feeding, what can be offered to provide nutrition?

A

NG Tube: short term feeding that can give all fluids and food or used for supplementary feeding to patient’s usual intake

PEG/RIG/PEGJ/RIGJ: medium to long term feeding placed into stomach or jejunum by endoscopy or radiologically

TPN: nutrition and fluid into central line when GI tract obstructed or not working (diseased or short gut)

65
Q

What are the disadvantages of each of the following feeding methods:

  • NG Tube
  • PEG
  • RIG
  • TPN
A

NG Tube: risk of aspiration from food removed but can still aspirate on saliva, need to check pH or CXR everytime before feeding to check in stomach, patient has to mobilise with drip

- PEG: risk of aspiration from saliva, have to pierce stomach so risks, cannot be done endoscopically if poor anatomy

- RIG: have to be changed regularly due to balloon, easily dislodged

- TPN: line sepsis, liver dysfunction

66
Q

What is the BMR of a standard man and woman?

A

Amount of energy expended at rest. It provides enough energy for the functioning of the vital organs only

67
Q

What is refeeding syndrome?

A

Presents as acute congestive HF due to fluid shifts associated with reintroduction of carbohydrate after prolonged starvation. Also respiratory and neurological dysfunction

  • Hypophosphataemia
  • Hypokalaemia
  • Hypomagnesaemia

Refeeding syndrome is a potentially life-threatening complication that can occur when someone who has been malnourished starts eating again, especially if reintroduced too quickly or with too much food. It’s essentially a metabolic shock caused by the sudden shift in how the body uses nutrients. Here’s a breakdown of what happens:

During malnutrition:

The body adapts to conserve energy by slowing down metabolism and shutting down certain processes.
This leads to depletion of electrolytes (minerals like potassium, magnesium, and phosphorus) and other essential nutrients.
Glucose levels in the blood also drop, leading to muscle breakdown for energy.
Upon refeeding:

When food is reintroduced, the body tries to switch back to normal metabolism, but it lacks the resources (electrolytes, nutrients) to do so efficiently.
A sudden influx of glucose triggers insulin release, causing the body to shift from using fat for energy back to glucose.
This rapid shift can cause imbalances in electrolyte and fluid levels, potentially leading to serious complications.
Key factors contributing to refeeding syndrome:

Severity and duration of malnutrition: The more severe and prolonged the malnutrition, the higher the risk.
Rate of refeeding: Introducing food too quickly or in large quantities increases the risk.
Underlying medical conditions: Certain conditions like liver disease or heart failure can worsen the effects.
Consequences of refeeding syndrome:

Electrolyte imbalances can lead to heart arrhythmias, muscle weakness, seizures, and even coma.
Fluid shifts can cause edema (swelling) and affect lung function.
Vitamin and mineral deficiencies can worsen existing symptoms and impair organ function.
Preventing refeeding syndrome:

Early identification of individuals at risk is crucial.
Gradual refeeding with carefully planned, calorie-controlled diets is essential.
Close monitoring of electrolyte levels and other vital signs is necessary.

68
Q

What patients are at high risk of developing refeeding syndrome?

A
  • Prolonged starvation
  • Severely malnourished
69
Q

What is the pathophysiology of refeeding syndrome?

A

When in starvation insulin levels drop and phosphate levels drop

When carbohydrate is reintroduced insulin rapidly rises to produce glycogen and this requires phosphate. Phosphate, Mg, K are forced into cells and Na out causing fluid shifts

Hypophosphataemia reduces ATP production so impaired function of cardiac muscle. Also 2,3-DGP is reduced in red cells so cannot deliver oxygen to tissues as well

70
Q

How can we prevent refeeding syndrome?

A

- Reintroduction of food slowly e.g 5-10kcal/kg/day and check Mg, PO4 and K+ until full feeding

  • Before feeding replenish phosphate levels with IV phosphate infusion

- Multivitamins

71
Q

What is contained in the solution for parenteral nutrition?

A
  • Water
  • Glucose
  • Nitrogen
  • Lipid
  • Electrolytes
  • Vitamins and trace elements

Given over 12-24h by central venous catheter

72
Q

What are some of the complications of parenteral nutrition?

A
73
Q

How do you calculate the calories in a PN bag?

A

(Nitrogen x 25) + Lipids + Glucose

74
Q

What are some clinical signs of anorexia nervosa?

A
  • Lanugo
  • Low BMI
  • Calluses on knuckles
  • Eroding teeth
75
Q

What are some complications with anorexia nervosa?

A
  • Osteoporosis
  • Fractures
  • Hypoglycaemia
  • Hypothermia
  • Liver failure
  • Infection
76
Q

If a patient with anorexia nervosa attends hospital they are usually very unwell, how should you start feeding these patients?

A

Keep low threshold for abx therapy

  • Get dietician review ASAP
  • IV phosphate replacement and Vit B complex
  • Slow NG tube feeding under MHA
77
Q

This patient has UC, what does the x-ray show?

A

- Toxic megacolon

- Mucosal oedema due to visible bowel wall

  • Not visible on this x-ray but always look for proximal constipation
78
Q

What antibiotic prophylaxis should you give to patients with ascites following SBP?

A

Ciprofloxacin

79
Q

What are some risk factors for an upper GI bleed?

A
  • Age
  • NSAIDs and anticoagulants
  • Coagulation disorders
  • Liver disease
80
Q

How do you do a nutritional assessment in patients with IBD?

A
  • Dietary intake history
  • BMI
  • Body composition
  • MUST
81
Q

What are some differentials for bloody diarrhoea?

A
  • IBD
  • Infective: shigella, e.coli, giardia
  • Malignancy
  • Diverticulitis
82
Q

What are some important questions to ask about nausea and vomiting to determine the underlying cause?

A
  • What is in the vomit? e.g coffee grounds, feculent
  • Timing? e.g morning could be pregnancy, post food ulcer
83
Q

What investigations should you do for acute nausea and vomiting?

A

- Bloods: FBC, U+Es, LFTs, Ca, Glucose, Amylase

- ABG: check for alkalosis as loss of acid from stomach

- Plain AXR: if suspect bowel obstruction

- Endoscopy: if suspect upper GI bleed

84
Q

What is the treatment for acute nausea and vomiting?

A
  • Try oral antiemetics but if cannot keep down give IV
  • Check if dehydrated and give IV fluid replacement with K+
85
Q

What are some causes of a high MCV?

A
  • Alcohol
  • Low B12 and folate
  • Hypothyroidism
  • Myelodysplasia
  • Reticulocytosis (e.g from bleed)
  • Azathioprine
  • Pregnancy
86
Q

What are some differentials for diarrhoea (not including infective differentials)?

A
  • IBD
  • IBS
  • Coeliacs
87
Q

Which parasite causes steatorrhoea?

A

Giardia - treat with metronidazole

88
Q

Why does C.Diff have a high recurrence rate?

A
  • Spore formation
  • If recurrence give Fidoxamicin
89
Q

What are some symptoms of carcinoid syndrome?

A
  • Wheezy breathlessness
  • Watery diarrhoea
  • Flushing

Give octreotide

90
Q

What are some causes of low sodium?

A
  • SIADH
  • Thiazides
  • Addison’s
  • Dehydration with water replacement
  • Cirrhosis
  • Heart failure
91
Q

What is the albumin gradient?

A

Serum Albumin - Ascitic Albumin

If <11 this is normal, cannot have cirrhosis!!!!!

>11 means portal HTN and cirrhosis

92
Q

What antibiotic can cause drug induced cholestasis?

A

Co-amoxiclav and Flucloxacillin

93
Q

What is transferrin like in HH?

A

All transferrin saturated, if less than 50% saturation cannot be HH

94
Q

What is the significance of a raised transferrin?

A

It is an acute phase protein so can be raised for lots of reasons

95
Q

What are some causes of clubbing?

A
  • Cirrhosis
  • Lung cancer
  • ILD
  • Bronchiectasis
  • Coealiacs
  • IE
  • Idiopathic

NOT COPD!! misdiagnosis or lung cancer if in COPD

96
Q

How can you distinguish between severe constipation and LBO?

A

Will have no flatulence in LBO

97
Q

What is the difference in the pain in pancreatitis and SBO?

A
  • Pancreatitis pain constant
  • SBO colickly
98
Q

What does bowel urgency indicate?

A

RECTAL DISEASE