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Year 3 Medicine > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Why is lactulose used in the management of hepatic encephalopathy?

A

Reduce generation of ammonia by bacteria in the gut and reduce the absorbability of ammonia from the gut

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2
Q

What is the optimum endoscopic therapy for bleeding oesophageal varicies?

A

VBL

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3
Q

What are the clinical features of each grade of hepatic encephalopathy?

A

Grade 0 No abnormality
Grade 1 Alterations in behaviour, mild confusion, disordered sleep
Grade 2 Lethargy, moderate confusion, asterixis
Grade 3 Somnolent but can be roused
Grade 4 Coma

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4
Q

What is the gold standard investigation for diagnosing coeliac disease?

A

Endoscopy with duodenal biopsy

To be performed after positive serology

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5
Q

What is seen on duodenal biopsy in coeliac disease?

A

Villous atrophy
Crypt hyperplasia
Increase in intra-epithelial lymphocytes

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6
Q

What are the first line serology investigations for coeliac disease?

A

Total IgA

IgA tissue transglutaminase (TTG)

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7
Q

Does hepatitis A increase the risk of hepatocellular carcinoma?

A

No

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8
Q

What is the treatment for Hep A?

A

Supportive, usually self limiting

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9
Q

Features of Crohn’s disease

A 
Affects anywhere from mouth to anus
Skip lesions
Inflamation is transmural
Fissuring ulcers
Lymphoid and neutrophil aggregates
Non caseating granulomas
Increased incidence in smokers
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10
Q

Features of UC

A 
Always affects the rectum, extends proximally
Continuous
Mucosa and sub mucosa inflammation only
Crypt abscesses 
Decreased incidence in smokers
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11
Q

What tests should be considered for patients with a change in bowel habit?

A

Blood tests - FBC (anaemia, raised platelet count), U&E (derrange electorlytes, AKI), CRP (inflmation, can indicate IBD)
Stool tests - culture (r/o infective collitis), faecal calprotectin (active IBD)
Simple imaging - AXR (proximal constipation, toxic megacolon)
Endoscopy - felxi sig (safest test in bloody diarrhoea), colonoscopy (to look for proximal disease), capsule endoscopy (visualise small bowel mucosa)
Cross sectional imaging - CT abdomen (acute compliactions), MRI enterography (small bowel crohn’s, fistulas), MRI rectum (perianal crohns)

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12
Q

Why do patients with acute IBD need prophylactic heparin when staying in hospital?

A

High risk of VTE

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13
Q

What are the rescue therapies in UC?

A

Ciclosporin
Biologics (e.g. Infliximab)
Surgery

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14
Q

What are the rescue therapies for Crohns disease?

A

IV hyrdocortisone - first line
Biologics (e.g. Infliximab)
Surgery

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15
Q

What is used to maintain remission in UC

A

Mesalazine (5-ASAs)

IF INEFFECTIVE
Sulfasalazine
Azathiprine and biologics (e.g. Infliximab)

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16
Q

What drugs are used to maintain remission in Crohn’s disease?

A

Azithioprine

Biologics (e.g. Infliximab)

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17
Q

What histological changes will be seen in UC?

A

Non-granulomatous inflammation of the mucosa and submucosa
Crypt abcesses
Goblet cell hypoplasia
Pseudopolyps

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18
Q

What is the cardinal feature of UC?

A

Bloody diarrhoea

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19
Q

Symptoms of UC

A

Proctitis, inflmmation confinded to the rectum only
Bloody diarrhoea
PR bleeing
Mucus discharge (PR)
Increased frequency and urgency of defecation
Tenesmus
Systemic symptoms: malaise, anorexia, low-grade pyrexia

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20
Q

Features of severe UC

A 
>6 bowel movements per day
Visable Blood
Pyrexia
Tachycardia
ESR>30
Anaemia
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21
Q

Complications of UC

A 
Toxic megacolon
Colorectal carcinoma
Osteoperosis
Puchitis
Bowel perforation
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22
Q

What curative surgery can be used to manage UC?

A

Total proctocolectomy

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23
Q

Why do patients with UC typically require segmental bowel resection, typically needing a subtotal colectomy defunctioning stoma?

A

In a flare of IBD primary anastomosis is not adivsed

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24
Q

AXR features of UC flares

A

Mural thickening, thumbprinting, lead-pipe colon

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25
Q

What are some extra-intestinal manifestations of IBD?

A

MSK - enteropathic arthritis (large joints such as sacroilliac), clubbing (Crohns- metabolic bone disease)
Skin - erthema nodosum, (Crohn’s, pyoderma gangrenosum)
Eyes - episcleritis, anterior uveitis, iritis
Hepatobillary - primary sclerosing cholangitis (more with UC), cholangiocarcinoma, gallstones
Renal - Renal stones in Crohn’s disease

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26
Q

Which IBD has a cobblestone appearance?

A

Crohn’s

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27
Q

What are the biggest risk factors for Crohn’s disease?

A

Family history

Smoking

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28
Q

How does Crohn’s disease present?

A

Episodic abdominal pain
Diarrhoea, which may contain blood or muscous
Systemic symptoms: malaise, anorexia, low-grade fever
Malnourishment and malabsorption (failure to thrive in children)
Oral Apthous ulcers
Perianal disease including perianal abscess

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29
Q

Wha

A
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30
Q

Gold standard investigation for Crohns?

A

Colonoscopy

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31
Q

What score can be used to grade the severity of Crohn’s disease?

A

Montreal score:

Age, behaviour, location

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32
Q

How might CT imaging be usefull in Crohns?

A

Bowel obstruction from stricturing
Bowel perfoation
INtra abdominal collections

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33
Q

How is treatment in haemochromatosis monitored?

A

Ferritin and transferrin saturation

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34
Q

What triad does chronic mesenteric ischaemia often present with?

A

Severe, colicky post-prandial abdominal pain
Weight loss
Abdominal bruit

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35
Q

What will the acid base status of a patient with mesenteric ischemia be and why?

A

Metabolic acidosis

Low bicarbonate

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36
Q

What triad may mesneteric ischemia present with?

A

CVD
Soft tender abdomen
High lactate

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37
Q

In hepatomegaly secondary to right sided heart failure, what is found on examination of RUQ?

A

Pulsatile, smooth, tender, liver edge

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38
Q

Why should colonoscopy be avoided in patients with severe colitis?

A

Risk of perforation

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39
Q

What may be seen on CT abdomen of a patient with pancreatic cancer?

A

Double duct sign - simultaneous dilatation of the common bile duct and pancreatic ducts

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40
Q

What kind of duct dilation will primary sclerosing cholangitis cause?

A

Intra-hepatic

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41
Q

In a patient with previous hepatitis B immunisation, what will be seen on serology?

A

anti-HBsAg positive

All others negative

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42
Q

What will be positive on Hep B serology in patients who have had previous Hep C (>6months ago)?

A

anti-HBc

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43
Q

What will hep B serology show if a patient is carrying Hep B?

A

HBsAg positive

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44
Q

What anti-emetic should be avoided in bowel obstruction?

A

Avoid metoclopramide in bowel obstruction

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45
Q

What is the most common organism found on ascitic culture?

A

E coli

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46
Q

What is the ‘M rule’ in primary billary cholangitis?

A

IgM
anti-Mitochondrial antibodies, M2 subtype
Middle aged females

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47
Q

In autoimmune hepatitis which antibodies and immunoglobins will be positive/raised?

A

Antinuclear antibody
Anti smooth muscle antibody
IgG

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48
Q

Clinical features of IBS?

A 
Bloating 
Change in bowel habit
Abdominal pain and distension, relieved by defecation 
Mucus in stool 
Back pain
Urinary symptoms 
Fatigue 
Symptoms made worse by eating
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49
Q

How should a suspected perianal fistula be investigated?

A

MRI pelvis

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50
Q

What iron study findings will be present in patients with untreated heriditory haemochromatosis?

A

Raised transferritin saturation
Raised ferritin
Low total iron binding capacity

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51
Q

Which part of the colon is most likely to be affected by ischemic colitis?

A

Splenic flexure

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52
Q

What is Wilson’s disease?

A

Wilson’s disease is an autosomal recessive disorder characterised by excessive copper deposition in the tissues.

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53
Q

What liver pathology can arise secondary to Wilson’s disease?

A

Copper deposition leading to hepatitis or cirrhosis

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54
Q

What physical findings may be present in a patient with Wilson’s disease?

A

Kayser-Fleischer rings (green-brown rings in the periphery of the iris)
Blue nails

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55
Q

What psychiatric symptoms can Wilson’s disease cause?

A

Psychosis

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56
Q

Dysphagia equally to both solids and liquids from the outset is characteristic of what?

A

Achlasia

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57
Q

How may haematomochrosis present clinical features wise?

A 
Bronze appearance of the skin
Hepatomegaly 
Bilateral joint pain due to chondrocalcinosis of the joints
Weakness 
Hyperglycaemia
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58
Q

What is used to screen for Wilson’s disease?

A

Serum Caeruloplasmin

reduced

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59
Q

Best measure of acute liver failure?

A

Prothrombin time

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60
Q

What does a high SAGG indicate

A

Portal hypertension

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61
Q

What is the acute management of severe alcoholic hepatitis?

A

corticosteroids

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62
Q

What is Peutz-Jeghers syndrome

A

Peutz-Jeghers syndrome is an autosomal dominant condition characterised by numerous hamartomatous polyps in the gastrointestinal tract

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63
Q

What drugs tend to cause drug induced cholestasis?

A

combined oral contraceptive pill
antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas
fibrates

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64
Q

What kind of GI bleed does a high urea suggest?

A

Lower GI bleed

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65
Q

What is the The Mackler triad for Boerhaave syndrome?

A

Subcutaneous emphysema
Thoracic pain
Vommting

(Oesophageal rupture)

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66
Q

Why are anti-motility drugs like loperamide, sometimes used to treat diahorrea, contraindicated in patients with Crohns during a flare up?

A

Anti-motility drugs, such as loperamide, should be avoided in acute attacks, as these can precipitate toxic megacolon.

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67
Q

Why should colonoscopic surveillance be offered to people with Crohns, and under what circumstance?

A

Due to increased risk of colorectal malignancy, colonoscopic surveillance is offered to people who have had the disease for over ten years and have over one bowel segment affected.

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68
Q

When is surgical management indicated in Crohn’s?

A

Failed medical management
Strictures
Perforation
Surgeons will take a bowel sparing approach

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69
Q

What surgeries may be performed to manage Crohns?

A

Ileocaecal resection
Small or large bowel resection
Surgery for peri-anal disease (I&D, laying open of fistulae, seton insertion)
Stricturoplasty

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70
Q

Complication of Crohn’s disease?

A 
Fistula (enterovesical, enterocutaneous, rectovaginal)
Stricture formation
Recurrent perianal fistulae
GI mallignancy 
Malabsorption
Osteoperosis
Gallstones
Renal stones
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71
Q

What is the stepwise progression of alcoholic liver disease?

A
  1. Alcohol related fatty liver
  2. Alcoholic hepatitis
  3. Cirrhosis
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72
Q

How long does it take to reverse alcohol related fatty liver after alcohol cessation?

A

2 weeks

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73
Q

Is alcoholic hepatitis reversable?

A

With permanent abstinence

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74
Q

Is alcoholic liver cirrhosis reversable?

A

No but alcohol cessation will prevent further damage

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75
Q

What is the reccomended limit of alcohol consumption?

A

14 units a week, over 3+ days

No more than 5 units in one day

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76
Q

What is the CAGE question used to screen for alcohol missuse?

A

Cut down
Annoyed
Guilty
Eye opener

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77
Q

What score on the AUDIT questionaire indicated harmful alcohol use?

A

8 or more

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78
Q

What are the complications of alcohol abuse?

A 
Alcoholic liver disease
Cirrhosis
Hepatocellular carcinoma (2* to cirrhosis)
Dependence, withdrawal
WKS, wernicke korsakoff syndrome
Pancreatitis
Alcoholic cardiomyopathy
Clotting problems
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79
Q

What may be found on examination of a patient with liver disease?

A 
Jaundice
Hepatomegaly
Spider naevi
Palmar erythema
Gynaecomastia
Brusing (abnormal clotting)
Ascites
Capur meduase (engoged superficial epigastric veins)
Asterixis
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80
Q

What may be seen on LFTs in alcoholic liver disease?

A

Elevated transaminases (AST, ALT) with abnormal AST:ALT ratio
Particularly raised gamma-GT
Low albumin
Elevated bilirubin

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81
Q

In liver disease, what does low albumin indicate?

A

Reduced synthetic function of the liver

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82
Q

What AST:ALT is indicative of alcoholic liver disease?

A

> 2

ie. AST is twice that of ALT

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83
Q

What might be abnormal in the FBC of a patient with alcoholic liver disease?

A

Raised MCV

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84
Q

Why may U&Es be derranged in a patient with alcoholic liver disease?

A

Hepatorenal syndrome

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85
Q

Why are CT and MRI useful in liver disease?

A

Look for fatty infiltration of the liver, hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes, ascities

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86
Q

When is liver biopsy reccomended in patients with alcoholic liver disease?

A

When steroid treatment is being considered

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87
Q

What is the role of endoscopy in suspected portal hypertension?

A

Assess for and treat oesophogeal varicies

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88
Q

What scan can be used to check the elasticity of the liver and assess the degree of cirrhosis?

A

FIbroscan (USS)

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89
Q

What scan can be used to check the elasticity of the liver and assess the degree of cirrhosis?

A

FIbroscan (USS)

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90
Q

How will fatty changes in the liver be visable on USS?

A

Increased echogenicity

91
Q

What is the general management of alcoholic liver disease?

A

Immediate alcohol cessation
Consider a detoxication regime
Nutritional support with vitamins (particulary thiamine) and a high protein diet
Steroids improve short term outcomes (over 1 month) in severe alcholic hepaitits
Treat infection and GI bleeding
Treat complications of cirrhosis (portal HTN, varices, ascities, hepatic encephalopathy)
3 months after cessation of alcohol liver transplant can be considered

92
Q

What are the symptoms of alochol withdrawal and at what point to they occur?

A

6-12 hours: tremor, sweating, headache, craving an anxiety
12-24 hours: hallucinations
24-48 hours: seizures
24-72 hours: delirium termens

93
Q

What drug is used in portal HTN?

A

Propanolol

94
Q

What is delirium tremens?

A

Medical emergency associateds with alcohol withdrawal

95
Q

How does delirium tremens present?

A 
Acute confusion
Severe agitation
Delusions and hallucinations
Tremor
Tachycardia
HTN
Hyperthermia
Ataxia 
Arrythmias
96
Q

What is the pathophysiology of delerium tremens?

A
  1. Alcohol use: Inhibition of the electrical activity of the brain
    This is due to stimulation of GABA receptors and inhibition of NMDA (glutamate) receptors
  2. Chronic alcohol use - GABA system down regulated, glutamate system upregulated to balance the effects of alcohol
  3. When alcohol is removed from the system GABA under functions and glutamate over functions, cuasing an extreme excitability of the brain with excess adrenergic activity.
97
Q

In particular what vitamin needs to be replaced in alocholics?

A

Thiamine (vit B1)

Given as pabrinex IV in alcohol withdrawal. ( B1, B2, B6, nicotinamide, vitamin C and glucose)
Given as oral suplimentation at a lower dose afterwards

98
Q

What complications can arise from vitamin B1 (thiamine) deficiency?

A

Wernicke-Korsakoff Syndrome (WKS)

  1. Wernicke’s encephalopathy
  2. Korsakoff syndrome
99
Q

What benzodiazapine is given as first line to combat alcohol withdrawal?

A

Chlordiazepoxide

Given over 5-7 days, titrated down

100
Q

Clinical features of Wernicke’s encephalopathy?

A

Confusion
OCulomotor disturbances
Ataxia

Medical emergency, high mortality rate if left untreated

101
Q

Clinical features of Korsakoffs syndrome?

A 
Memeory impairment (retrograde and aterograde)
Behavioural change

Often irreversable

102
Q

What are the most common causes of liver pathology where ALT>500

A

Viral (consider hep A and E)
Ischemia
Toxicity (usually paracetomol)
Autoimmune

103
Q

What are the most common causes of liver pathology where ALT 100-200?

A

Non-alcoholic steatohepaititis
Autoimmune hepaitits
CHronic viral hepatitis
Drug induced liver injury

104
Q

What cholestatic pathologies cause duct dilations?

A

Gallstones

Mallignanacy

105
Q

What cholestatic pathologies cause non-dilated ducts?

A

Alcoholic hepaititis
Cirrhosis - PBC, PSC, Alcohol
Drug induced liver injury (antibioitics - co-amoixclav)

106
Q

What is included in the liver screen?

A

Hepatitis B&C serology (+A and E in acute disease with marked ALT rise)
Iron studies (ferritin and transferrin saturation)
Autoantibodies (AMA&SMA) and immunoglobins
Consider caeuruloplasmin if under 30 years
Alpha-a-antityrpsin
Coeliac serology
TFTs, lipids, glucose

107
Q

What are the symptoms of coeliac disease?

A 
Loose stools 
Bloating
Wind 
Abdominal cramps
Weight loss
Dermatitis herpetiformis
108
Q

What are the potential complications of coeliac disease?

A 
Small bowel cancer
Small bowel lymphoma 
Osteoperosis
Gluten Ataxia
Gluten neuropathy
109
Q

What enzyme is raised in the bloods of most patients with coeliac disease (although not diagnostic in adult patients)

A

tTG (tissue transglutaminase)

110
Q

What is histologically seen in coeliac disease?

A

Villous atrophy

Intra-epithelial lymphocytosis

111
Q

When red flag symptoms or atypical symptoms are associated with dysphagia/weight loss/new onset at older age what investigation is indicated?

A

OGD should be considered

112
Q

What causes oesphageal dysphagia?

A

Physical obstruction

Neuromuscular problem

113
Q

Neuromuscular causes of oesophageal dysphagia

A

Achalasia
Dysmotility
Prebyoesophagus

114
Q

Obstructive causes of oesophageal dysphagia?

A

Tumor
Benign (peptic) stricture
Inflmattion from oesophagitis

115
Q

What is used to exclude obstrcutive causes of oesophageal dysphagia?

116
Q

What investigations will identify neuromuscular causes of oesophageal dysphagia?

A

Barium swallow

Oesophageal manometry

117
Q

What is the medical term for a painful swallow?

A

Odynophagia

118
Q

How are benign oesophogeal stricture treated?

A

Dilatation

119
Q

How are oesophogeal cancers managed definitively?

A

Stenting

Surgical resection

120
Q

What is oro-pharangeal dysphagia?

A

Difficulty getting the food to mouth

121
Q

What usually causes oro-pharyngeal dysphagia?

A

Problems coordinating the muscles that move the food bolus to the back of the mouth, as the result of a neurological disease such as a stroke

122
Q

What should be examined/investigated in a patient with oro-pharangeal dysphagia?

A

Cranial nerve examination
SALT assesment
A video-fluroscopy

123
Q

What are the functions of the liver?

A 
Stores glycogen
Releases glucose
Absorbs fats, fat soluble vitamins & iron
Manufactures cholesterol
Dissolves dietary fats
Breakdown product of haemoglobin 
Manufactures most clotting products
Drug excretion (/activation)
Alcohol breakdown
Kupfer cells engulf antigens
Albumin and binding protin manufacture
124
Q

Risk factors for liver disease

A 
Blood transfusions (prior to 1990 in the UK)
IVDU
Operations/vaccinations with dubious sterile procedures
Sexual exposure
Medication (prescribed/self prescribed)
FH of liver disease, diabetes, IBD
Obesity
Features of metabolic syndrom 
Alcohol dependency/abuse
Forigen travel
125
Q

Examples of causes of acute liver disease (resolves within 6 months)

A 
Hep A
Hep E
CMV
EBV
Drug induced liver injury
126
Q

What is thrombocytopenia (in liver pathology) a sensitive marker for?

A

Liver fibrosis

127
Q

USS findings that suggest liver cirrhosis?

A

Coarse tecture
Nodularity
Splenomegaly
Ascites

128
Q

Most common causes of chronic liver disease?

A

Alcoholic liver disease
Non-alcoholic steatohepatitis
Viral hepatitis (B&C)

129
Q

Less common but important causes of chronic liver disease?

A 
Autoimmune hepatitis
Primary bililary cholangitis
Primary sclerosing cholangitis
Haemachromatosis
Wilsons disease and anti LKM autoimmune hepatitis (both in adolescents and young adults)
130
Q

How does familial adenomatosis polyposis coli present?

A

Often seen on endoscopy with the formation of hundreds of polyps within the colon
Patients will inveitibly develop carcinoma

131
Q

What is the presence of varicies on endocsopy in a patient with chronic liver disease also diagnostic of?

A

Liver cirrhosis

132
Q

Primary prophylaxis for patients with varices?

A

Beta blockers

Oesophageal variceal ligation for medium/large varices

133
Q

How is ascites treated pharmacologically?

A

Sprinolactone

134
Q

How can tense ascites be treated?

A

Paracentesis

135
Q

Other conditions which patients with liver cirrhosis are at risk of, and what screening can be performed?

A

Osteoperosis, dexascan

Hepatocellular carcinoma, alpha-fetoprotein and USS every 6 months

136
Q

Other conditions which patients with liver cirrhosis are at risk of, and what screening can be performed?

A

Osteoperosis, dexascan

Hepatocellular carcinoma, alpha-fetoprotein and USS every 6 months

137
Q

What is performed in a diagnostic ascitic tap (to look for SBP)?

A

Cell count and MC&S

138
Q

What are the factors used to calculate a MUST score, for screening for malnutrition?

A

BMI (18.5-20 = 1. <18.5 = 2)
Unexplained weight loss in past 3-6 months (5-10% = 1, >10% = 2)
If patient is acutely ill and there has been or is likely to be no nutritional intake for >5 days (2)

139
Q

What MUST score indicated medium risk?

140
Q

What MUST score indicates high risk?

141
Q

First step in managing malnutrition?

A

High calorie options
Reduced mealtime interruptions
Food fortification
Dietitian referral

142
Q

Options to feed patients with an unsafe swallow?

A

NG Tube
PEG/RIG/PEGJ/RIGJ
Parenteral Nutrition (macronutrients and micronutrients given via PICC or Hickman line)

143
Q

Risks of TPN?

A

Sepsis

Liver dysfunction

144
Q

How can you ensure that you have correctly placed an NG tube?

A

Test pH of aspirate

CXR

145
Q

How can you ensure that you have correctly placed an NG tube?

A

Test pH of aspirate

CXR

146
Q

Which tubes can be used for longer-term enteral feeding into the stomach?

147
Q

Which tubes can be used for longer-term enteral feeding into the small bowel?

A

PEG-J

RIG-J

148
Q

What is important to clarify in a history from a patient with a GI bleed?

A

Is it haematemesis? (fresh blood, vomited)
Coffee ground vomit (?altered blood)
Melaena (black, tarry sticky stool)
Fresh PR bleeding (lower GI bleed, or brisk upper GI bleed in a very haemodynamically unstable patient?

149
Q

Risk factors for an upper GI bleed?

A 
Varices
Chronic liver disease (/stigmata of)
NSAIDs
Antiplatelets
Anticoagulants
150
Q

What scores can be used to assess GI bleeding?

A

ROCKALL score

Blatchford score

151
Q

What score is used to predict the need for intervention in a GI bleed (such as blood transfusion, therapeutic endoscopy)?

A

The Blatchford score

152
Q

What score is used to predict the need for intervention in a GI bleed (such as blood transfusion, therapeutic endoscopy)?

A

The Blatchford score

153
Q

What investigations may be helpful in a GI bleed?

A

FBC (Hb, platelet count (thrombocytopenia in liver disease))
U&Es - a raised urea supports a diagnosis of upper GI bleeding
Clotting - abnormal clotting
Group and Save (Cross match if haemodynamically unstable) in case blood transfusion required
LFTs - chronic liver disease (but normal does not rule out)

154
Q

What is the quickest way to get a haemoglobin result in a haemodynamically unstable?

A

Venous Blood Gas

155
Q

How is Variceal bleeding managed?

A

Fluid resuscitation followed by blood if heamodynamically unstable (note that systolic BP is often low in pts with cirrhosis)
IV Terlipression
IVAbx
Endocscopy with band ligation (or Liton tube or TIPSS if unsucsessful)

156
Q

What does TIPSS stand for?

A

trans-jugular, intrahepatic porto-systemic shunt

157
Q

Is there evidence for giving PPI before an endoscopy?

A

Not in a non-variceal bleed

158
Q

How might paracetamol overdose present?

A 
Asymptomatic
N&V
Loin pain
Haematuria and proteinuria
Jaundice
Abdominal pain
Coma
Severe metabolic acidosis
158
Q

How might paracetamol overdose present?

A 
Asymptomatic
N&V
Loin pain
Haematuria and proteinuria
Jaundice
Abdominal pain
Coma
Severe metabolic acidosis
159
Q

What is the name of the toxic symptoms that builds up during a paracetamol overdose?

A

NAPQI

N-acetyl-p-benzoquinone-imine

160
Q

How is paracetamol overdose managed when ingestion was less than one hour ago and the dose was over >150mg/kg

A

Activated charcoal

161
Q

How is paracetamol overdose managed when the ingestion was staggered, or when ingestion was over 15 hours ago?

A

Start N-acetylcysteine immediatley

162
Q

How is paracetamol overdose managed when ingestion was less than 4 hours ago?

A

At FOUR HOURS take a level and treat with N-acetylcysteine based on level

163
Q

How is paracetamol overdose managed when ingestion was 4-15 hours ago?

A

Take immediate level and treat based on level

164
Q

What bloods should be obtained in paracetamol overdose?

A 
Paracetamol level
FBC
U&Es
INR
VBG
165
Q

How should an anyphlactoid reaction to NAC be managed?

A

Stopping the infusion temporarily, restarting at a lower rate
(Not a true anaphylactic reaction)

166
Q

In which patients, due to their increased risk of paracetamol overdose toxicity, be given NAC immediately?

A

Patients on long-term enzyme inducers
Regular alcohol excess
Pre-existing liver disease
Glutathione-deplete states: eating disorders, malnutrition, HIV

167
Q

What is the triple therapy for H-pylroi erradication?

A

Amoxicillin, clarithromycin and a PPI twice daily for seven days

168
Q

Why do patients with CLD often have excorations?

A

Excorations as a result of scratching secondary to pruritis associated with raised serum bilirubin, generally preceeds jaundice

169
Q

What can be used to reduce pruritus in chronic liver disease?

A

Colestyramine, a bile acid sequestriant, to reduce raised serum bilirubin

170
Q

What are the two main causes of high urea - ‘protein meal’?

A

The 2 major causes of this includes a high-protein diet or an upper
gastrointestinal bleed, the latter occurring as a result of gut bacteria breaking down blood proteins.

171
Q

What blood markers are indicative of refeeding syndrome?

A

Low phosphate
Low magnesium
Low potassium
Hyperglycaemia

172
Q

How is refeeding syndrome managed?

A

Slow introduction of food

Thiamine replacement

173
Q

What electrolyte imbalance can severe vomiting cause?

A

Metabolic alkalosis (by product of increased acid secretion in the stomach)
Hypokalaemia (due to increased potassium wasting in the kidneys in exhcnage for proton retention to combat the alkalosis)
Hypochloraemia (due to loss of chloride in the vomit)

174
Q

How do you calculate units of alcohol?

A

Strength (ABV) x Volume (ml)

175
Q

Where is vitamin B12 absorbed?

A

Terminal ileum

176
Q

Where is folic acid, nicotinamide and vitamin D absorbed?

177
Q

Clinical signs indicative of portal HTN?

A

Caput medusae

Splenomegaly

178
Q

What is Budd-Chiari Syndrome?

A

Hepatic vein obstruction
Classic triad: severe abdominal pain, ascites, tender hepatomegaly
Primary if there is hepatic vein thrombosis
Often seen in pts with haematological conditions (e.g polycythaemia ruba vera), or pro-coagulable states
Secondary if there is external compression of hepatic vein (secondary to a liver, renal, or adrenal tumour)

179
Q

Gold standard for diagnosis of Budd-Chiari Syndrome?

A

Diagnosis is an abdnominal USS with Doppler studies?

180
Q

Common electrolyte distrubance in Crohn’s disease?

A

Hypomagnesia due to malabsorption and diahorrea

181
Q

Why can re-feeding syndrome lead to arrythmias, diarrhoea and seizures?

A

Hypomagnesaemia

Severe hypophosphatemia

182
Q

What is the

183
Q

What is gastroparesis?

A

Syndrome of delayed gastric emptying in the absence of mechanical obstruction.

184
Q

Features of gastroperisis?

A 
Post-prandial fullness
Nausea 
Vomiting,
Bloating
Abdominal pain
185
Q

Causes of gastroperisis?

A

Poorly controlled diabetes leading to longer period of hyperglycemia, causing automonic neuropathy - which can affect the gastric system and caused delayed gastric emptying
Post bariatric surgery
Parkinson’s disease
Scleroderma

185
Q

Causes of gastroperisis?

A

Poorly controlled diabetes leading to longer period of hyperglycemia, causing automonic neuropathy - which can affect the gastric system and caused delayed gastric emptying
Post bariatric surgery
Parkinson’s disease
Scleroderma

186
Q

What is toxic megacolon?

A

Toxic megacolon occurs when a section of the colon becomes inflamed and damaged, resulting in a breakdown of the mucosa and exposure of the muscular component of the bowel wall. As a result, there is a loss of tone and motility in the affected section that can result in a build-up of faecal matter and consequently complications such as infection and perforation.

187
Q

What type of infective gastroenteritis is associated with profuse vomiting and short incubation period?

A

Staphylococcus aureus gastroenteritis

188
Q

Pain from gastric ulcers

A

Pain from gastric ulcers is classically exacerbated by food, and maximal within 30 minutes to an hour of eating a meal

189
Q

Diagnosis of gastric ulcers?

190
Q

First line management of staggered paracetmol overdose?

A

In patients who have taken a staggered overdose first line treatment is with N-acetylcysteine regardless of the time from ingestion.

191
Q

When is it appropriate to take blood paracetamol level and wait for result before initiating treatment in a pt with paracetomol overdose?

A

This is the correct course of action in patients with an overdose of <150mg/kg that has been ingested within a 1 hour period - not staggered,

192
Q

When should activated charcol be given in paracetmol overdosE?

A

In a non-staggered overdose presenting within an hour when the GCS is 8 or higher

193
Q

What is type of anaemia does iron def cause?

A

Iron deficiency causes a microcytic, hypochromic anaemia.

194
Q

What type of anaemia does B12 def cause?

A

B12 deficiency can cause a macrocytic anaemia.

195
Q

Anaemia in malnourished pts?

A

In patients with marked generalised malnutrition (as is clear from this patient’s history) a normocytic anaemia can prevail. This is due to mixed effects of iron deficiency (which normally causes a microcytic anaemia) and B12 +/- folate deficiency (which normally causes a macrocytic anaemia).

196
Q

How long before testing must a pt be eating gluten when investigating coeliac disease?

A

Patients must eat gluten for at least 6 weeks before they are tested

197
Q

What landmark determines upper vs lower gi bleed

A

The definition of an Upper GI Bleed is a haemorrhage with an origin proximal to the ligament of Treitz

198
Q

Histology in coeliac

A

Villous atrophy
Crypt hyperplasia
Intraepithelial lymphocytes

199
Q

Rash in coealiac?

A

Dermititis herpetiformis

200
Q

Second line treatment of hepatic enchephalopathy?

A

Rifaximin
Embolisation of portosytemic shunts
Liver transplant

201
Q

Precipiates of heptatic enchepaholopathy

A 
Bleeding (upper GI)
Infection
Constipation
Electrolyte imbalance 
Protein intake
Sedation
Renal failure
202
Q

Anaemia in coeliac disease?

A
  1. Anaemia of chronic disease (microcytic)
  2. B12 def (macrocytic)
  3. Folate def (macrocytic)

Therefore pts will have either microcytic anaemia (iron def dominates) or normocytic (due to mixture of all 3)

203
Q

What does vitamin B1 (thiamine) deficiency cause?

A

Cognative impairment

204
Q

Causes of koilonychia (spoon shaped nails)

A

Iron deficiency anaemia (e.g. Crohn’s disease)
Lichen planus
Rheumatic fever

205
Q

Causes of leukonychia (whitening of nails)

A

Nailbed trauma
Hypoalbuminaemia (e.g. end-stage liver disease, protein-losing enteropathy)
Chemotherapy

206
Q

What is seen on bariam swallow in achlasia?

A

Birds beak appearance

207
Q

What antibodies can cause pernicious anaemia?

A

Anti-intrinsic factor antibodies - bind to intrinsic factor made by parietal cells in gastric fundus so Vitamin b12 reduced absorption in terminal illeum

208
Q

What gastroenterology condition is associated with anti-microbial antibodies?

209
Q

What gastroenterology condition is associated with intrinsic factor antibodies?

A

Pernicious anemia

210
Q

What gastroenterology condition is associated with anti-glandin antibodies?

211
Q

What gastroenterology condition is associated with anti smooth muscle antiboides?

A

Autoimmune hepaitis

212
Q

How to assess if alcohol intake is problematic?

A

CAGE
Felt need to Cut down
Do you get Annoyed by people critising your drinking
Do you ever feel Guilty about drinking
Do you ever need a drink Early in the morning

213
Q

Macrocytosis?

A

Loss of central hollowness on blood film

RBC appear higher

214
Q

Causes of macrocytosis?

A

B12 def
Folate def
Liver disease

215
Q

Which liver enzymes are most associated with alochol liver diesase?

A

Gamma GT

ALT

216
Q

Alchol withdrawal timeline?

A
  1. 8 hours - anxiety, nauseua, insomina abdopain
  2. Days 1-3 High blood presuure increase body temp
  3. 1 week Hallucination fever seizures and agidtation
217
Q

Gilbert syndrome

A 
Autosomal recessibe
20-60 bilirubin
Associated flares with stress
Jaundice with no other abnormality
Reassure and discharge
218
Q

Secondary prophylaxis of hepatic encephalopathy?

A

Lactulose and rifaximin

219
Q

Globus pharygis

A

Globus pharyngis (also known as globus hystericus) is the persistent sensation of having a ‘lump in the throat’, when there is none

220
Q

What is pellagra?

A

Def of vit B3 (nican)

Dementia, dermatitis, death

221
Q

If a patient with ulcerative colitis has had a severe relapse or >=2 exacerbations in the past year they should be given what?

A

either oral azathioprine or oral mercaptopurine to maintain remission

222
Q

Urine dip where Urobilinogen is absent. Bilirubin is strongly positive?

A

Conjugated bilirubin only = post hepatic jaundice

Year 3 Medicine (8 decks)

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