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ISCE prep > Gastrointestinal Examination > Flashcards

Gastrointestinal Examination Flashcards

1
Q

What is xerostomia?

A

Dry mouth

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2
Q

What is halitosis?

A

Bad breath due to gingivitis, dental or pharyngeal infection

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3
Q

What is dysgeusia?

A

Altered taste sensation

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4
Q

What is cacageusia?

A

Foul taste sensation eg. rotting food

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5
Q

What is haematochezia?

A

Rectal bleeding

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6
Q

Causes of a painful mouth

A

Idiopathic- recurrent aphthous ulcers
Infections- candidiasis, dental sepsis, herpes simplex virus
Trauma
Systemic disorder
Skin disorder- pemphigoid, lichen planus, pemphigus vulgaris, erythema multiforme

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7
Q

Dyspepsia that is worse on an empty stomach and relieved by eating is likely to be

A

Peptic/ duodenal ulceration

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8
Q

Likely causes of odynophagia

A

Oesophagitis or candidiasis

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9
Q

Severe abdominal pain sudden onset that rapidly becomes progressively generalised and constant is likely…

A

Hollow viscus perforation, ruptured AAA or mesenteric infarction

Clues may be in the previous history- constipation from colorectal cancer or diverticular disease, dyspepsia

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10
Q

Severe abdominal pain sudden onset radiating to the back

A

Ruptured or dissecting abdominal aortic aneurysm

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11
Q

Angor animi

A

The feeling of impending death

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12
Q

Achalasia

A

Lower oesophageal sphincter fails to relax normally- dysphagia with both solids and liquids

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13
Q

Neuromuscular causes of dysphagia

A

Achalasia, pharyngeal pouch, myasthenia gravis, oesophageal dysmotility

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14
Q

Oral causes of dysphagia

A

Tonsillitis, glandular fever, peritonsillar abscess, painful mouth ulcers, pharyngitis

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15
Q

Symptom checklist in dysphagia

A 
Painful or painless?
Intermittent or progressive?
Length of history and onset?
Solid or liquid or both?
Previous Hx of dysphagia or heartburn?
Where does food stick?
Complete obstruction with regurgitation?
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16
Q

Gastric outlet obstruction causes what type of vomiting?

A

Projectile non-bilious vomiting

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17
Q

Neurological causes of vomiting

A 
Raised ICP- SOL, meningitis
Labyrinthitis 
Meniere's disease 
Migraine
Vasovagal syncope, shock, fear and severe pain
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18
Q

Causes of ascites

A

Common- hepatic cirrhosis with portal hypertension, intra-abdominal malignancy with peritoneal spread
Uncommon- hepatic vein occlusion (Budd-Chiari syndrome), constrictive pericarditis and other right sided heart failure, hypoproteinaemia (nephrotic syndrome), tuberculosis peritonitis, pancreatitis

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19
Q

Causes of bloody diarrhoea

A

IBD, colonic ischaemia or infective gastroenteritis

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20
Q

What is Mallory- Weiss syndrome?

A

Forceful retching and vomiting ruptures oesophageal mucosa causing the vomiting of fresh blood

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21
Q

Coffee ground vomit

A

Blood that has been degraded by gastric pepsin is vomited

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22
Q

Causes of melaena

A

Upper GI bleeding that is then passed through the system- excessive alcohol ingestion causing erosive gastritis, Mallory-Weiss tear, bleeding oesophageal varices, peptic ulceration

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23
Q

Causes of rectal bleeding

A 
Haemorrhoids
Anal fissure
Colorectal polyps/ cancer
IBD
Ischaemic colitis
Complicated diverticulitis disease
Vascular malformation
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24
Q

Causes of angular stomatitis

A

Denture problems, candidiasis, iron deficiency or B12 deficiency

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25
Q

ALARMS symptoms

A 
Anaemia
Loss of weight
Anorexia
Recent progression or onset of symptoms
Melaena/ haematemesis
Swallowing difficulty
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26
Q

Differentials for dyspepsia

A 
Non-ulcer dyspepsia
Duodenal/ gastric ulcer
Duodenitis 
Oesophagitis/ GORD
Gastric malignancy 
Gastritis
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27
Q

When should upper GI endoscopy be done in dyspepsia cases?

A

Dysphagia
>55
ALARMS symptoms

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28
Q

Treatment for H. pylori

A

PPI

2 antibiotics eg. Clarithromycin and amoxicillin

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29
Q

Treatment of GORD

A

Conservative- lifestyle, smoking cessation, weight loss, small regular meals, avoidance of causative food and drink, raise the bed head, avoid eating 3 hours before bed
Medical- antacids, PPI, H2 receptor antagonist, avoid drugs that can affect oesophageal motility or that damage mucosa
Surgical- laparoscopic Nissen fundoplication to increase resting LOS pressure

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30
Q

Symptoms of GORD

A

Retrosternal burning
Discomfort after eating, straining, lying
Belching
Acid regurgitation
Odynophagia from oesophagitis or ulceration
Extra-oesophageal such as nocturnal cough

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31
Q

Acute management of an upper GI bleed

A

A-E assessment
Senior involvement
High flow oxygen and protection of the airway
Insert 2 large bore cannulae
Bloods- FBC, U&Es, LFT, clotting and crossmatch
IV fluids whilst waiting for crossmatched blood
Catheter insertion and monitor hourly fluids
CXR, ECG, ABG
Transfuse if significant Hb drop (<70)
Correct clotting abnormality
If suspicion of varices then give terlipressin
Broad spectrum abx cover
Monitor obs hourly until stable
URGENT ENDOSCOPY (clips, cautery, adrenaline)
If endoscopic control fails then surgery or emergency mesenteric embolisation may be needed
If uncontrollable oesophageal variceal bleeding then Sengstaken-Blakemore tube may compress varicies

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32
Q

Risk score used for upper GI bleeds

A

Rockall score

Predicts risk of rebleeding and death

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33
Q

Causes of portal hypertension (leading to gastro-oesophageal varices)

A

Pre-hepatic- thrombosis
Intra-hepatic- cirrhosis (80% in UK), schistosomiasis (commonest worldwide), sarcoid, myeloproliferative diseases
Post-hepatic- budd-chiari syndrome, right heart failure, constrictive pericarditis

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34
Q

Management of gastro-oesophageal varices

A

Endoscopic banding or sclerotherapy
Non-selective beta blockade
TIPS for resistant varices

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35
Q

Causes of bloody diarrhoea

A

Campylobacter, Shigella, Salmonella, E. coli, amoebiasis
UC, Crohn’s, colorectal cancer, colonic polyps
Colitis (ischaemic)

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36
Q

Treatment of C. difficile in mild and severe cases

A

Mild- metronidazole

Severe- vancomycin

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37
Q

Proctalgia fugax

A

Temporary pain around the anal area of unknown origin

Usually intense muscle spasm- similar to levator ani syndrome

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38
Q

Endocrine causes of constipation

A

Hypercalcaemia

Hypothyroidism

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39
Q

Description of UC pathology

A

Continuous inflammation limited to the mucosa and distal to the ileocaecal valve
Haemorrhagic colonic mucosa +/- pseudopolyps formed by inflammation

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40
Q

What kind of UC flare?
5 motions/per day, some rectal bleeding
70-90BPM

A

Moderate

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41
Q

Complications of UC

A

Acute- toxic megacolon with risk of perforation
VTE, hypokalaemia
Chronic- colonic cancer, risk related to disease activity and extent- surveillance colonoscopy important

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42
Q

Treatment of UC
Mild
Moderate
Severe

A

Mild- 5-ASA PR eg mesalazine for distal disease or PO if more extensive. Steroids may be used in addition

Moderate- 4-6 motions per day but otherwise well(ish)
oral prednisolone to induce remission, maintain on 5-ASA

Severe- admission, IV hydration, eletrolyte replacement, IV steroids- hydrocortisone 100mg, VTE prophylaxis, stool MC&S to exclude infection

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43
Q

Description of Crohn’s disease pathology

A

Chronic inflammatory condition characterised by transmural granulomatous inflammation affecting any part of the gut.
Skip lesions
Rose thorn ulceration

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44
Q

Clinical features of Crohn’s disease

A 
20-40 years old classically 
Diarrhoea
Generally unwell- fever, malaise, fatigue, anorexia
Failure to thrive 
Weight loss 
Abdominal pain

Signs: adbo tenderness/ mass, perianal abscess, fistulae, skin tags, anal strictures, clubbing, skin and joint involvement, anterior uveitis/ iritis/

45
Q

Crohn’s disease treatment

A

SMOKING CESSATION
mild-moderate- Prednisolone 40mg and then taper off, dietary advice
Severe- Admission for IV hydration/ electrolyte replacement, IV steroids- hydrocortisone or methylpred, VTE prophylaxis, MC&S to exclude infection
Daily FBC, ESR, CRP, U&E and AXR, blood transfusions and nutritional support if necessary
If improving switch to oral pred, consider biologic use

Peri-anal disease:
TNF-alpha, other immunosuppressants, oral antibiotics, local surgery and seton insertion

46
Q

Biologic therapies that can be used in Crohn’s disease

A

Azathioprine
Methotrexate
TNF-alpha- infliximab, adalimumab
Other monoclonal antibodies

47
Q

Genetic associations with coeliac disease

A

HLA DQ2 is 95%
HLA DQ8 are the rest
Autoimmune disease
Dermatitis herpetiformis

48
Q

Presentation of coeliac disease

A

Any age but peaks in childhood and 50-60
Steatorrhoea, diarrhoea, abdo pain, bloating, nausea and vomiting, aphthous ulcers, angular stomatitis, weight loss, fatigue, osteomalacia, failure to thrive

49
Q

Antibody in coeliac disease and further test to confirm

A 
Anti-tissue transglutaminase and total IgA check to exclude subclass deficiency 
Duodenal biopsy to confirm (whilst on a gluten containing diet)
50
Q

Mucosal changes in coeliac disease

A

Villus atrophy
Crypt hyperplasia
Intra-epithelial WBC’s

51
Q

Complications of coeliac disease

A 
Anaemia
Dermatitis herpetiformis 
Osteopenia/osteoporosis 
Hyposplenism- flu and pneumococcal vaccine
Increased risk of malignancy
52
Q

Things to rule out when diagnosing IBS

A 
Chronic >6 months
Query if age >60 
No weight loss, anorexia, waking at night with pain/ diarrhoea, mouth ulcers
Abnormal CRP, ESR
FH of ovarian or bowel cancer (CA-125)
Endometriosis- cyclical pain 
Stool culture
FBC, LFTs, U&Es, coeliac serology
53
Q

Clinical features of scurvy

A

Poor, pregnant or odd diet
Anorexia, cachexia, gingivitis, loose teeth, halitosis, bleeding from gums or into joints, bladder, gut, muscle pain, weakness, oedema

54
Q

Beriberi

A

Thiamine deficiency
Wet beriberi- heart failure with general oedema
Dry beriberi- neuropathy

55
Q

Classical triad of pellagra

A

Lack of nicotinic acid- B3- niacin

Diarrhoea, dementia and dermatitis

56
Q

Causes of acute pancreatitis

A 
Gallstones
Ethanol
Trauma
Steroids
Mumps and other infections
Autoimmune
Scorpion bites
Hypercalcaemia, hypertriglyceridaemia, hypothermia
ERCP
Drugs
57
Q

Tests for pancreatic cancer query

A

CA19-9
Bloods show cholestatic jaundice
Imaging- US or CT- pancreatic mass, biliary tree dilatation or hepatic mets

58
Q

What is a Whipple’s resection?

A

Pancreatoduodenectomy

59
Q

Gilbert’s syndrome

A

Decreased UGT-1 activity resulting in unconjugated hyperbilirubinaemia
Often presents with intermittent jaundice in young adulthood during infections

60
Q

Crigler-Najjar syndrome

A

Inherited unconjugated hyperbilirubinaemia presenting in the first days of life
Mutation in the UGT enzyme causing absent (1) or impaired (2) bilirubin excretion

61
Q

Causes of unconjugated hyperbilirubinaemia

A

Haemolysis, ineffective erythropoiesis
Impaired hepatic uptake- drugs- paracetamol, rifampicin, ischaemic hepatitis
Impaired conjugation
Physiological neonatal

62
Q

Causes of conjugated hyperbilirubinaemia

A

Hepatocellular dysfunction- viruses- hepatitis, CMV, EBV, drugs, alcohol, cirrhosis etc
Impaired hepatic excretion- PBC, PSC, gallstones, pancreatic CA, compression, cholangiocarcinoma,

63
Q

Questions to ask the patient in jaundice

A 
Blood transfusions
IV drug use
Piercings 
Tattoos 
Sexual activity
Travel
Jaundiced contacts
FH
Alcohol 
Medications
64
Q

Investigations for jaundice

A

Haematology- FBC, clotting, blood film, Coomb’s test, haptoglobins
Biochemistry- U&Es, LFTs, GGT, total protein, albumin, paracetamol levels
Microbiology- blood cultures, hepatitis serology
USS- bile duct dilatation, masses, gallstones

65
Q

‘Coagulopathy’ in terms of INR

A

> 1.5

66
Q

Causes of liver failure

A 
Infections- viral hepatitis- B,C, CMV, yellow fever, leptospirosis 
Drugs- paracetamol, isoniazid 
Toxins- deathcap
Vascular- Budd Chiari syndrome- occlusion of the hepatic veins
Alcoholic Liver Disease 
Non Alcoholic Fatty Liver Disease
PBC
PSC
Haemochromatosis 
Autoimmune hepatitis 
Alpha-1 antitrypsin deficiency 
Wilson's disease
Malignancy
Fatty liver of pregnancy
67
Q

Hepatic encephalopathy pathogenesis

A

Nitrogenous waste builds up from liver failure

Astrocytes mop up by conversion of glutamate to glutamine and this excess causes osmotic imbalance and cerebral oedema

68
Q

Signs of liver failure

A

Jaundice
Hepatic encephalopathy- incoherent, restless, confusion, asterixis, stupor
Asterixis
Signs of acute or chronic liver failure

69
Q

What is hepatorenal syndrome?

A

Cirrhosis+ ascites + renal failure

Abnormal haemodynamics result in renal vasoconstriction and hypoperfusion

70
Q

Treating ascites

A

Restrict fluid, low salt diet, weight daily, diuretics

71
Q

Signs of liver cirrhosis

A 
Leukonychia 
Telangiectasia
Clubbing
Palmar erythema
Dupuytren's contracture 
Spider naevi
Xanthelasma
Gynaecomastia 
Loss of body hair
Parotid enlargement- alcohol
Hepatomegaly (small in late disease)
Ascites
Splenomegaly
72
Q

Complications of liver cirrhosis

A

Hepatic failure: coagulopathy, hypoalbuminaemia, encephalopathy, sepsis, spontaneous bacterial peritonitis, hypoglycaemia
Portal hypertension- ascites, caput medusae, splenomegaly, oesophageal varices

73
Q

When should spontaneous bacterial peritonitis be considered?

A

Any patient with ascites that deteriorates very quickly

74
Q

Only definitive treatment for cirrhosis

A

Liver transplant

75
Q

Investigations once recovery from a HepB virus infection

A

Normal LFTs
Anti-HBs
Anti-HBc IgG

76
Q

Vaccinated against HepB virus

A

Anti-HBs

Normal LFTs

77
Q

What does HBeAg mean

A

Implies high infectivity, present 6-12 weeks after acute illness

78
Q

Hep C percentage of chronic silent infections

A

85%

79
Q

Managing alcoholic hepatitis

A 
Hospital admission
Stop alcohol consumption + alcohol withdrawal- long acting benzodiazepine- CIWA-Ar
IV vit K and pabrinex- B1
Optimise nutrition 
Daily weight, INR, LFT and U&Es
Steroids
80
Q

Antibody in primary biliary cholangitis

A

Anti-mitochondrial antibodies

81
Q

Signs of primary biliary cholangitis

A 
Jaundice
Skin pigmentation
Xanthelasma
Xanthomata
Hepatosplenomegaly
82
Q

Tests for primary biliary cholangitis

A

Raised ALP
Raised GGT
AMA
USS- exclude extrahepatic cholestasis

83
Q

Treatment for primary biliary cholangitis

A

Symptomatic- pruritus, diarrhoea, osteoporosis prevention, fat soluble vitamin ADEK prophylaxis
Ursodeoxycholic acid/ cholestyramine
Monitoring
Liver transplant for end-stage disease

84
Q

Primary sclerosing cholangitis who gets it, increased risk of…

A

Over 80% have IBD- usually UC
Men 30-40
Increased risk of cancers- yearly colonoscopy and ultrasound

85
Q

Antibodies in primary sclerosing cholangitis

A

ANA
SMA
pANCA

86
Q

Who does autoimmune hepatitis tend to affect?

A

Young or middle aged women in a bimodal distribution

87
Q

Antibodies likely to be positive in autoimmune hepatitis

A

ASMA

88
Q

Type 1 autoimmune hepatitis

A

80% of cases
Typically women <40
ASMA positive, IgG in 97%
25% have cirrhosis at presentation

89
Q

Type 2 autoimmune hepatitis

A

Children
Less treatable and more commonly progresses to cirrhosis
LKM1 antibodies
ASMA negative

90
Q

Management of autoimmune hepatitis

A

Immunosuppressant therapy- prednisolone
Azathioprine as steroid sparing agent to maintain remission
Liver transplant indicated for decompensated cirrhosis

91
Q

Associations of autoimmune hepatitis

A 
Pernicious anaemia 
UC
Glomerulonephritis
Autoimmune thyroiditis
Autoimmune haemolysis
DM
PSC
92
Q

Pathology of non-alcoholic fatty liver disease

A

Increased fat in the hepatocytes- steatosis

93
Q

Wilson’s disease pathology

A

Rare inherited disorder of copper excretion with excess deposition in the liver and CNS
Autosomal recessive

94
Q

Signs of Wilson’s disease

A

Children- liver disease- hepatitis, cirrhosis, fulminant liver failure
Young adults- CNS signs- tremor, dysarthria, dysphagia, dyskinesias, dystonias, dementia, parkinsonism, ataxia
Mood- depression, mania, labile emotions, personlity change
Cognitive deprivation
Kayser-Fleischer rings- copper deposition in iris

95
Q

Management of Wilson’s disease

A

Diet- avoidance of copper rich food
Lifelong penicillamine
Liver transplantation

96
Q

How can you tell if ALP is from bone or liver?

A

Other deranged LFTs, particularly GGT

97
Q

Alcoholic liver disease LFT classic

A

AST/ALT ratio is 2:1

98
Q

Suspected liver tumour investigations

A

Bloods- FBC, LFT, clotting, hepatitis serology, alpha-fetoprotein
US or CT to identify lesions and guide biopsy
ERCP and biopsy if cholangiocarcinoma suspected

99
Q

Two most common mutations for hereditary haemochromatosis

A

C282Y and H63D

100
Q

Signs of haemochromatosis

A 
Tiredness early on
Arthralgia 
Decreased libido
Slate grey skin
Signs of liver disease, cirrhosis
Bronze diabetes from iron deposition in the pancreas
101
Q

Management of haemochromatosis

A

Venesection
Well balanced diet
Avoid alcohol and uncooked seafood
Monitor LFTs and glucose

102
Q

Tests if suspecting A1AT deficiency

A

Serum A1AT levels low (but can be disguised by inflammation as it is an acute phase protein)
Lung function tests- obstructive picture (emphysema)
Liver biopsy

103
Q

Best imaging modality for acute diverticulitis

A

CT abdomen

104
Q

Symptoms of diverticulitis

A 
Altered bowel habit
Left-sided colic relieved by defecating 
Pyrexia
Increased CRP/ESR and WCC
Tender colon +/- localised or general peritonism
105
Q

Complications of diverticulitis

A 
Perforation
Haemorrhage
Fistulae
Abscesses 
Post-infective strictures
106
Q

Fissure-in-ano often if chronic found with a…

A

‘Sentinel pile’ or mucosal tag at the external aspect

107
Q

Treatment for fissure-in-ano

A

conservative- dietary fibre, fluids, stool softener and hygiene advice
5% lidocaine ointment and GTN ointment or topical diltiazem

108
Q

Treatment for fistula-in-ano

A

Fistulotomy and excision
High require a seton suture
Low need to be laid open to allow healing by secondary intention

109
Q

Symptoms of haemorrhoids

A

Bright red rectal bleeding (on wiping or coating stools)
Mucous discharge and pruritus ani
Anaemia may be severe

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