General gastro Flashcards

1
Q

What is acute upper gastrointestinal bleeding most commonly due to

A

Peptic ulcer disease

Oeseophageal varices

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2
Q

Risk assessment in upper gastrointestinal bleeding

A

Use the blatchford score at first assessment(admission risk marker - patients with 0 may be considered for early discharge)

Full rockall score after endoscopy

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3
Q

Immediate management of acute GI bleed

A

A-E resus
Platelet transfusion if actively bleeding
FFP if low fibrinogen or APTT elevated
Immediate endoscopy after resuscitation within 24 hrs

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4
Q

Why should PPIs not be prescribed in an acute GI bleed

A

Should not be prescribed until post-endoscopy as they may mask the site of bleeding

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5
Q

Management of variceal bleeding

A

terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e. before endoscopy)

band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices

transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures

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6
Q

Symptoms and signs of giardiasis

A
Asymptomatic 
Watery malodorous diarrhoea 
Abdominal cramps and distension 
Nausea 
Epigastric discomfort
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7
Q

What is giardiasis often accompanied by

A

Acquired lactose-intolerance

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8
Q

Transmission of giardiasis

A

Some trophozoites transform into environmentally resistant cysts that are spread by focal-oral route

Waterborne transmission is the major source of infection but transmission can occur from ingestion of contaminated food or direct person-to-person contact

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9
Q

Diagnosis of giardiasis

A

Enzyme immunoassay for antigen or molecular test for parasite DNA in stool

Microscopic examination of stool(characteristic trophozoites or cysts in stool are diagnostic)

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10
Q

Treatment for giardiasis

A

Metronidazole(warn to not drink alcohol to avoid disulfiram-like reaction)

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11
Q

What is Barrett’s oesophagus

A

Metaplasia of the lower oesophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium

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12
Q

What type of cancer does Barrett’s oesophagus predispose to

A

Oesophageal adenocarcinoma

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13
Q

Risk factors for Barrett’s oesophagus

A

GORD is the single strongest risk factor
male gender (7:1 ratio)
smoking
central obesity

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14
Q

Mx of Barrett’s oesophagus

A

endoscopic surveillance with biopsies(recommended for patients with metaplasia every 3-5 yrs)

high-dose proton pump inhibitor

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15
Q

Options if dysplasia of any grade is identified in the oesophagus

A

Endoscopic mucosal resection

Radiofrequency ablation

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16
Q

Most common site for UC

A

Rectum(inflammation always starts there)

Never spreads beyond ileocaecal valve

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17
Q

Initial presentation of UC

A
bloody diarrhoea
urgency
tenesmus
abdominal pain, particularly in the left lower quadrant
extra-intestinal features
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18
Q

Extra-intestinal features of UC

A
Pauciarticular arthritis 
Asymmetric erythema nodosum 
Episcleritis 
Osteoporosis 
PSC
Uveitis
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19
Q

Pathology features of UC

A

red, raw mucosa, bleeds easily
no inflammation beyond submucosa (unless fulminant disease)

widespread ulceration with preservation of adjacent mucosa which has the appearance of polyps

inflammatory cell infiltrate in lamina propria
neutrophils migrate through the walls of glands to form crypt abscesses

depletion of goblet cells and mucin from gland epithelium
granulomas are infrequent

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20
Q

What might a barium enema show in UC

A

loss of haustrations
superficial ulceration, ‘pseudopolyps’
long standing disease: colon is narrow and short -‘drainpipe colon’

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21
Q

Classification of UC

A

mild: < 4 stools/day, only a small amount of blood
moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)

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22
Q

What is proctitis

A

Inflammation of the rectum

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23
Q

Inducing remission in proctitis

A

topical (rectal) aminosalicylate: for distal colitis rectal mesalazine has been shown to be superior

if remission is not achieved within 4 weeks, add an oral aminosalicylate

if remission still not achieved add topical or oral corticosteroid

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24
Q

Inducing remission in proctosigmoiditis and left-sided ulcerative colitis

A

Topical aminosalicylate

If remission is not achieved within 4 weeks, an oral corticosteroid for 4 to 8 weeks in addition to the high-dose aminosalicylate should be offered.

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25
Q

Management of mild-to-moderate ulcerative colitis that is extensive

A

A topical aminosalicylate and a high-dose oral aminosalicylate

If remission is not achieved within 4 weeks, stop topical aminosalicylate treatment and offer a high-dose oral aminosalicylate and 4 to 8 weeks of an oral corticosteroid.

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26
Q

Treatment of acute severe ulcerative colitis

A

IV corticosteroids(hydrocortisone or methylpred)

Assess need for surgery

IV cyclosporin if corticosteroids are contra-indicated

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27
Q

Maintaining remission in mild, moderate or severe ulcerative colitis

A

maintenance therapy with an aminosalicylate is recommended in most patients. Corticosteroids are not suitable for maintenance treatment because of their side-effects.

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28
Q

Contra-indications of mesalazine

A

Blood clotting abnormalities

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29
Q

Side effects of aminosalicylates

A

Arthralgia
GI discomfort
Leucopenia
Nausea

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30
Q

Which parameters should be monitored before starting an oral aminosalicylate

A

Renal function

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31
Q

Trigger factors for UC

A

Stress
Medications(NSAIDs, antibiotics)
Cessation of smoking

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32
Q

Area commonly affected by crohn’s disease

A

Terminal ileum and colon

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33
Q

Complications of crohn’s disease

A
Intestinal strictures 
Abscesses in the wall of intestine 
Fistulae 
Anaemia 
Malnutrition 
Colorectal and small bowel cancers
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34
Q

Extra-intestinal features of crohn’s

A
Arthritis(pauciarticular) 
Asymmetric erythema nodosum 
Episcleritis(more common CD)
Osteoporosis 
Mouth ulcers 
Perianal disease
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35
Q

Ix for Crohn’s disease

A

raised inflammatory markers
increased faecal calprotectin
anaemia
low vitamin B12 and vitamin D

36
Q

Inducing remission in Crohn’s disease

A

glucocorticoids (oral, topical or intravenous) are generally used to induce remission. Budesonide is an alternative in a subgroup of patients

Enteral feeding with an elemental diet

37
Q

Second-line remission intervention in CD

A

5-ASA drugs (e.g. mesalazine) are used second-line to glucocorticoids but are not as effective
azathioprine or mercaptopurine* may be used as an add-on medication to induce remission but is not used as monotherapy. Methotrexate is an alternative to azathioprine

38
Q

Useful addition in refractory and fistulating CD

A

infliximab is useful in refractory disease and fistulating Crohn’s. Patients typically continue on azathioprine or methotrexate

39
Q

What can be used for isolated peri-anal disease in CD

A

Metronidazole

40
Q

Maintaining remission in CD

A

Stopping smoking is a priority

azathioprine or mercaptopurine is used first-line to maintain remission
+TPMT activity should be assessed before starting

methotrexate is used second-line

41
Q

What type of bacterium is C.diff

A

Gram positive rod

42
Q

What does C.diff cause

A

It produces an exotoxin which causes intestinal damage leading to a syndrome called pseudomembranous colitis.

43
Q

Risk factors for C.diff infection

A

Clindamycin
Second and third gen cephalosporins
PPIs

44
Q

Features of pseudomembranous colitis

A

diarrhoea
abdominal pain
a raised white blood cell count (WCC) is characteristic
if severe toxic megacolon may develop

45
Q

Diagnosis of pseudomembranous colitis

A

Is made by detecting Clostridium difficile toxin (CDT) in the stool

Clostridium difficile antigen positivity only shows exposure to the bacteria, rather than current infection

46
Q

1st line antibiotic for c diff infection

A

Oral vancomycin

47
Q

What is toxic megacolon

A

Nonobstructive dilation of the colon usually associated with systemic toxicity

48
Q

Common causes of toxic megacolon

A

IBDs

Infections(C diff, salmonella, CMV)

49
Q

Factors which precipitate toxic megacolon

A

Hypokalaemia
Medications(anticholinergics, opioids, antidepressants)
Barium enema
Colonscopy and bowel preparations

50
Q

Diagnosis of toxic megacolon

A

Radiographic evidence of the dilation of the colon greater than 6 cm

Fever 
Tachycardia 
Neutrophilic leukocytosis 
Anaemia 
Hypotension
51
Q

Management of toxic megacolon

A

Supportive
Abx(vancomycin and metronidazole)
Treat underlying cause
Surgical review

52
Q

Surgical management of toxic megacolon

A

current surgical treatment of choice in acute toxic megacolon is subtotal colectomy with ileostomy and either a Hartmann pouch, sigmoidostomy, or rectostomy

53
Q

What are pseudo polyps

A

Widespread ulceration in UC with preservation of adjacent mucosa which has the appearance of polyps

54
Q

What is GORD

A

acid from the stomach refluxes through the lower oesophageal sphincter and irritates the lining of the oesophagus

Oesophagus has a squamous epithelial lining making it more sensitive to the effects of stomach acid. The stomach has a columnar epithelial lining that is more protected against stomach acid

55
Q

GORD presentation

A
Heartburn
Acid regurgitation
Retrosternal or epigastric pain
Bloating
Nocturnal cough
Hoarse voice
56
Q

When should referral for endoscopy be made for GORD

A
Dysphagia (difficulty swallowing) at any age gets a two week wait referral
Aged over 55 (this is generally the cut off for urgent versus routine referrals)
Weight loss
Upper abdominal pain / reflux
Treatment resistant dyspepsia
Nausea and vomiting
Low haemoglobin
Raised platelet count
57
Q

Lifestyle advice for GORD

A
Reduce tea, coffee and alcohol
Weight loss
Avoid smoking
Smaller, lighter meals
Avoid heavy meals before bed time
Stay upright after meals rather than lying flat
58
Q

Mx of GORD

A

Gaviscon/Rennie
Omeprazole
Ranitidine as alternative to PPI

59
Q

Surgical mx of GORD

A

Surgery for reflux is called laparoscopic fundoplication. This involves tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter.

60
Q

Diagnosis of haemorrhoids

A

Bright red, painless rectal bleeding(on toilet paper/in toilet bowel)
Anal itching/irritation
Feeling of rectal fullness or incomplete evacuation on bowel movements
Soiling
Pain(not in internal)

61
Q

When should patients with haemorrhoids be admitted

A

Extreme pain

Internal haemorrhoids which have prolapsed

62
Q

Lifestyle advice to aid healing of the haemorrhoid

A

Advise on the importance of correct anal hygiene. The anal region should be kept clean and dry to aid healing and reduce irritation and itching. Recommend careful perianal cleansing and to pat (rather than rub) the area dry.

Avoid still withholding

63
Q

Mx of haemorrhoids

A

Simple analgesia

Topical haemorrhoids preparation(corticosteroids)

64
Q

Secondary care medical treatments for haemorrhoids

A

Rubber band ligation
Injection sclerotherapy
Infrared coagulation/photocoagulation

65
Q

Indications for liver transplant

A

acute liver failure or chronic liver failure. hepatocellular carcinoma.

66
Q

Factors suggesting unsuitability for liver transplant

A

Significant co-morbidities (e.g., severe kidney, lung or heart disease)
Current illicit drug use
Continuing alcohol misuse (generally 6 months of abstinence is required)
Untreated HIV
Current or previous cancer (except certain liver cancers)

67
Q

Scar associated with liver transplant

A

“rooftop” or “Mercedes Benz” incision along the lower costal margin for open surgery

68
Q

Post-transplant care

A
Lifelong immunosuppression 
Avoid alcohol and smoking
Treating opportunistic infections
Monitoring for disease recurrence (i.e. of hepatitis or primary biliary cirrhosis)
Monitoring for cancer
69
Q

Stages of non-alcoholic fatty liver disease

A

Non-alcoholic Fatty Liver Disease
Non-Alcoholic Steatohepatitis (NASH)
Fibrosis
Cirrhosis

70
Q

Risk factors for NAFLD

A
Obesity
Poor diet and low activity levels
Type 2 diabetes
High cholesterol
Middle age onwards
Smoking
High blood pressure
71
Q

Diagnosis of NAFLD

A

Liver ultrasound

72
Q

1st line recommended ix for assessing fibrosis in NAFLD

A

Enhanced liver fibrosis blood test (ELF)

Otherwise NAFLD fibrosis score

Then fibroscan

73
Q

Mx of NAFLD

A
Weight loss
Exercise
Stop smoking
Control of diabetes, blood pressure and cholesterol
Avoid alcohol
74
Q

Stages of alcoholic liver disease

A

Alcohol related fatty liver - build up of fat from drinking

Alcoholic hepatitis - usually reversible with permanent abstinence

Cirrhosis

75
Q

Complications of alcohol

A
Alcoholic Liver Disease
Cirrhosis  and HCC
Alcohol Dependence and Withdrawal
Wernicke-Korsakoff Syndrome (WKS)
Pancreatitis
Alcoholic Cardiomyopathy
76
Q

IX in alcoholic liver disease

A

FBC - raised MCV
LFTs - elevated ALT and AST, low albumin
Clotting - elevated prothrombin time
U&Es - deranged in hepatorenal syndrome

77
Q

Imaging ix in alcoholic liver disease

A

Fibroscan - assess degree of cirrhosis
Endoscopy
CT/MRI
Liver biopsy

78
Q

General mx of alcoholic liver disease

A
Alcohol cessation 
Detox regime 
Thiamine and high protein diet 
Steroids 
Liver transplant
79
Q

Alcohol withdrawal symptoms 6-12 hrs

A

tremor, sweating, headache, craving and anxiety

80
Q

Alcohol withdrawal symptoms 12-24 hrs

A

Hallucinations

81
Q

Alcohol withdrawal symptoms 24-48 hrs

A

Seizures

82
Q

Alcohol withdrawal symptoms 24-72 hrs

A

Delirium tremens

83
Q

Delirium tremens presentation

A
Acute confusion 
Hypertension 
Hyperthermia 
Tachycardia 
Delusions and hallucinations 
Tremor
84
Q

Which tool can be used to guide treatment in alcohol withdrawal

A

CIWA-Ar (Clinical Institute Withdrawal Assessment – Alcohol revised) tool

85
Q

Mx of effects of alcohol withdrawal

A

Chlordiazepoxide

IX high-dose B vitamins(pabrinex) followed by regular lower dose oral thiamine

86
Q

Features of wercicke’s encephalopathy

A

Confusion
Oculomotor disturbances (disturbances of eye movements)
Ataxia (difficulties with coordinated movements)

87
Q

Features of korsakoffs syndrome

A
Memory impairment (retrograde and anterograde)
Behavioural changes