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Electrolyte Disorders > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

What is Vincent’s infection?

A

Acute ulcerative gingivitis involving the interdental papillae. Treat with metronidazole.

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2
Q

What investigations would you do for dysphagia?

A

If suspicious of motility disorder = Barium Swallow

If suspicious of mechanical = OGD

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3
Q

What 3 infections most commonly affect the mouth?

A

Herpes Simplex Virus Type 1
Coxsackie A
Herpes Zoster

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4
Q

What can cause candidiasis?

A

Broad spec antibiotics, ill fitting dentures, aspirin, immunocompromised

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5
Q

What can predispose you to GORD?

A 
Increased abdominal pressure (pregnancy)
Low LOS pressure 
Delayed gastric emptying
Hiatus hernia
Obesity
Systemic Sclerosis
TCAs
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6
Q

When is OGD required in pts with GORD?

A

New onset over 55 yo

Pts with alarm symptoms (w/l, dysphagia,anaemia)

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7
Q

What would you do if patient does not respond to antacids?

A

24h pH intra-luminal monitoring

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8
Q

How do you manage GORD?

A

Diet and Lifestyle advice

Antacids (alginate, magnesium, aluminium)
PPIs (omeprazole, lansoprazole) - inhibit H/K/ATPase
H2-Receptor antagonists (ranitidine, cimetidine)

Surgery

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9
Q

In oesophageal spasm, what do you see on Barium swallow?

A

Cork-screw appearance

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10
Q

What causes Hiatus Hernia?

A

Sliding (95%) - gastro-oesophageal junction slides up

Para-oesophageal hernias - gastric fundus rolls up through the hiatus alongside the oesophagus

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11
Q

What is a common compliciation of long-standing GORD?

A

Stricture formation (treat with balloon dilatation)

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12
Q

What is the pathological change in Barrett’s Oesophagus?

A

Dysplasia - Squamous epithelium becomes columnar

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13
Q

What is the risk of Barrett’s?

A

Developing adenocarcinoma (NOT squamous)

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14
Q

What protocol is followed if dysplasia is found on endoscopy?

A

Low-grade = repeat endoscopy in 6months + high-dose PPIs

High-grade = repeat 3 monthly with high-dose PPIs if no visible lesion. If visible nodular lesions, then endoscopic resection for histopathological staging.

Radio-frequency ablation is the preferred method of endoscopic treatment.

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15
Q

What causes achalasia?

A

Impaired relaxation of the lower oesophageal sphincter

LOS pressure is elevated in >50% of cases

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16
Q

How do you treat achalasia?

A

Endoscopic balloon dilatation

Heller’s cardiomyotomy

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17
Q

Where in the oesophagus are adenocarcinomas more likely to be found?

A

Lower 1/3 + cardia

Squamous most likely in the middle 1/3

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18
Q

What investigations for oesophageal tumour?

A

OGD and tumour biopsy
+/- Barium swallow
Staging is via CT scan

Treat with resection

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19
Q

What stimulates acid secretion in the stomach?

A

Histamine working on the parietal cells

Parietal cells also release intrinsic factor

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20
Q

What causes the release of Histamine?

A

Acetylcholine and Gastrin via the enterochromaffin cells

Therefore ACh, Gastrin and Histamine cause release of Intrinsic factor

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21
Q

What inhibits histamine and gastrin release?

A

Somatostatin (so this stops acid production)

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22
Q

What is the function of intrinsic factor?

A

Absorbs vitamin B12 in terminal ileum

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23
Q

What are the functions of the stomach?

A

Reservoir for food
Emulsification of fat + mixing gastric contents
Secretion of intrinsic factor
Absorption

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24
Q

What is H.Pylori?

A

Gram -ve spiral shaped bacteria

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25
Q

How do you diagnose H.Pylori?

A 
Breath test (C-Urea) - also used to see if infection eradicated after treatment
Stool antigen

Antral biopsy - Rapid urease CLO test (INVASIVE)

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26
Q

What are the complications of H.Pylori?

A

Chronic gastritis
Peptic ulcer disease
Gastric B cell lymphoma
Gastric cancer

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27
Q

How do you treat H.Pylori?

A

PPI-Triple therapy - all twice a day for 14 days

Omeprazole (20mg) + Metronidazole (400mg) + Clarithromycin (500mg)

Omeprazole + Amoxicillin (1g) + Clarithromycin

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28
Q

Why do NSAIDs cause ulcers?

A

Reduced PG production via blocking COX-1 which usually gives mucosal protection

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29
Q

What relationship to food do peptic ulcers have?

A

Duodenal cause symptoms when pt is hungry and typically at night

Gastric usually cause symptoms after eating

Epigastric pain, relieved by antacids, nausea, heartburn, flatulence

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30
Q

What investigations for ulcer-type symptoms?

A

Pts < 55 = non-invasive H.Pylori testing (stool, breath)

Pts > 55 or alarm symptoms/signs (W/L, dysphagia, vomitting, GI bleed, epigastric mass)

If pt undergoes endoscopy, then biopsy needed to distinguish between malignant and benign

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31
Q

How do you manage peptic ulcers?

A

Eradicate H.Pylori with triple therapy (if thats the cause)

If non H.Pylori, then give PPIs and stop any NSAIDs/aspirin until ulcer is gone, then can start again WITH PPI if needed. If not possible to stop, switch to COX-2 inhibitor.

Follow-up endoscopy plus biopsy is done for all Gastric ulcers to exclude malignancy

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32
Q

What are the causes of peptic ulcer disease?

A

NSAIDs, H.Pylori, Steroids, Aspirin

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33
Q

What are the complications of ulcers?

A

Perforation
Gastric outlet obstruction
Haemorrhage

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34
Q

What is Curling’s ulcer?

A

Ulcer caused by a burn in the stomach

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35
Q

What are RFs for gastric cancer?

A

H.Pylori, chronic gastritis, tobacco smoking, high salt diet, pernicious anaemia

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36
Q

Where do gastric cancers most commonly occur?

A

Antrum of the stomach (usually adenocarcinoma)

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37
Q

What investigations would you perform in suspected gastric cancer?

A

Gastroscopy + biopsy is initial investigation of choice

CT, EUS and laparoscopy then used to stage the tumour

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38
Q

What other types of gastric tumours are there (other than adenocarcinoma) ?

A

GISTs

Gastric lymphoma

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39
Q

What are common causes of upper GI bleeding?

A 
Peptic Ulcers
Mallory-Weis syndrome
Gastric varices
Reflux Oesophagitis
Drugs - NSAIDs / Alcohol
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40
Q

How do you assess risk in a patient with GI bleed?

A

Rockall score

Looks at Age, BP + Pulse, Co-morbidities, Endoscopic stigmata, Diagnosis

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41
Q

What is pre-endoscopy drug therapy in a pt with upper GI bleed?

A

Stop aspirin, Warfirin, NSAIDS
Speak to cardiology regarding clopidogrel and aspirin
Reverse INR if severe enough
Give high-dose PPI if high-risk

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42
Q

What is a Mallory-Weiss tear?

A

Tear of the mucosa at oesophagogastric junction

History of vomiting preceding haematemesis suggests this pathology

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43
Q

What is the management of an upper GI bleed?

A 
Resuscitation 
Assess risk (Rockall score)
Pre-endoscopy drug therapy
Endoscopy
Treat based on cause (endoscopic haemostasis, surgery)
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44
Q

What antigens are associated with coeliac disease?

A

HLA DQ2 and HLA DQ8

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45
Q

What are the typical histological features of coeliac disease?

A

Villous atrophy
Crypt hyperplasia
Chronic inflammatory markers

46
Q

What investigations would you perform in coeliac disease?

A

Serum antibodies - tTG antibodies and EMA antibodies (less specific)

Distal duodenal biopsy - for definitive diagnosis

FBC - anaemia is seen in 50% cases

DXA - due to increased risk of osteoporosis

47
Q

Which part of gluten causes the problems seen in coeliac disease?

A

Alpha-gliadin

48
Q

What is the management of coeliac disease?

A 
Life-long gluten free diet
Pneumococcal vaccine (coeliac associated with hyposplenism)
49
Q

What are the complications of coeliac disease?

A

T-Cell lymphoma

50
Q

Which individuals should be tested for coeliac?

A

Autoimmune disease - T1DM, Thyroid, Addison’s
IBS
Unexplained osteoporosis
Down’s and Turner’s syndrome

51
Q

What is dermatitis herpetiformis?

A

Linked to coeliac disease
Itchy, symmetrical eruptions of vesicles on extensor surfaces due to IgA
Pts have gluten sensitivity, so gluten-free diet

52
Q

What is tropical sprue?

A

Diarrhoea, steatorrhoea and megaloblastic anaemia
Pt has been to a tropical area
Small bowel mucosal biopsy shows similar features to coeliac
Treat with folic acid and tetracycline

53
Q

What is a complication of bowel resection?

A

Small bowel syndrome - require parenteral nutrition

54
Q

TB of the small intestine most commonly affects…

A

Ileocaecal valve

55
Q

What is Whipple’s disease?

A

Rare, bacterial infection caused by Tropheryma whipplei
Abdo pain, fever, steatorrhoea, lymphadenopathy, arthritis
Treat with co-trimoxazole

56
Q

What are carcinoid tumours?

A

Arise from enterochromaffin cells which are seretonin producing

Symptoms are therefore due to raised 5-hydroxytryptamine

Symptoms from GI carcinoid tumours only arise if mets to the liver, as 5-HT drains into hepatic vein without being metabolised by liver

Flushing, wheezing, diarrhoea, abdo pain

Blood will show high levels of 5-HIAA

Treat with somatostatin analogue - cyproheptadine (inhibits seretonin)

Surgical resection

57
Q

What is Peutz-Jeghers syndrome?

A

Autosomal Dominant

Mucocutaneous pigmentation and GI polyps

58
Q

What is the role of smoking cigarettes in IBD?

A

Protective in U.C, risky for Crohn’s

59
Q

What are the macroscopic differences of Crohn’s and U.C?

A

Crohn’s - Any part of the GI tract, Oral and perianal disease, skip lesions, deep ulcers and fissures causing cobblestone appearance.

U.C - Affects only colon, begins in rectum and extends proximally, continuous involvement, red mucosa that bleeds easily

60
Q

What are the microscopic differences of Crohn’s and U.C?

A

Crohn’s - Transmural inflammation and granulomas present

U.C - Mucosal inflammation, no granulomata, goblet cell depletion, crypt abscesses

61
Q

What are the features of IBD?

A

Diarrhoea, abdominal pain, pain on defecation, w/l

Bloody diarrhoea with mucus often seen in U.C
Systemic features seen in relapse of U.C

62
Q

What are the extra-intestinal manifestation of IBD?

A

Clubbing
Eyes - Uveitis, conjunctivitis
Joints - Arthralgia, arthritis, ank spond
Skin - Erythema nodosum, Pyoderma gangrenosum
Liver - Fatty liver, hepatitis, cirrhosis, sclerosing cholangitis
Kidney - stones
DVT

63
Q

What investigations would you order for IBD?

A

Bloods, Cultures - blood + stool,
Flexible sigmoidoscopy +/- rectal biopsy
Colonoscopy
Small bowel imaging - barium follow through or video capsule endoscopy

64
Q

What investigation would you do urgently if a patient came in with acute severe colitis?

A

Plain abdominal X-Ray - identifies toxic dilation of colon

65
Q

What is the medical management of Crohn’s?

A

Steroids for moderate/severe disease
5-ASA more useful in U.C but occasionally used
Azathioprine to maintain remission in pts with regular relapses
Metronidazole in severe perianal disease
Anti-TNF antibodies are used for pts resistant to steroids

66
Q

What is the medical management of U.C?

A

Aim to induce a remission

Mild = Prednisolone 40mg  + Mesalazine
Moderate = Prednisolone  + 5-ASA (sulfasalazine, mesalazine)
Severe = admit

Remember to taper steroids

Azathioprine is reserved for those who relapse often (>2 courses of steroids in a year)

Anti-TNF antibodies are used for pts resistant to steroids
Infliximab, Adalimubab

67
Q

What is the management of severe colitis (after admission) ?

A

Blood and stool cultures x 3, AXR, Bloods

Nil by Mouth, IV fluids + correct electrolyte imbalances

Hydrocortisone IV 100mg 6 QDS
LMWH

If improves after 5 days, switch to oral prednisolone and 5-ASA. If not then give IV ciclosporin.

Close monitoring (vital signs QDS at least)

68
Q

What is the management of severe colitis (after admission) ?

A

Blood and stool cultures x 3, AXR, Bloods

Nil by Mouth, IV fluids + correct electrolyte imbalances

Hydrocortisone IV 100mg 6 QDS
LMWH

If improves after 5 days, switch to oral prednisolone and 5-ASA. If not then give IV ciclosporin.

Close monitoring (vital signs QDS at least, stool charts)

69
Q

When would surgical intervention (colectomy) be needed for UC?

A 
Perforation
Massive haemorrhage
Toxic dilatation
Failure to response to medical management
Failure to grow (in children)
70
Q

What are the complications of IBD?

A 
Stricture formation
Toxic dilation of colon +/- perforation
Abscess formation
Fistulae and Fissures
Colon cancer
71
Q

What are the rare side-effects of 5-ASA (sulfasalzine) ?

A

Steven-Johnson syndrome

Acute pancreatitis

72
Q

What are the potential side-effects of Azathioprine?

A

Bone marrow suppression

Acute pancreatitis

73
Q

What are the alarm symptoms associated with constipation?

A

Sensation of incomplete evacuation
Rectal bleeding
Recent onset in over 50s

74
Q

How do you diagnose and treat Diverticulitis?

A

Diagnosed via CT scan

Treat with abx - Metronidazole and a Cephalosporin)

75
Q

The risk of a polyp turning malignant increases with:

A 
Size > 1cm
Number
Sessile (worse) vs Pedunctulated 
Level of dysplasia
Villous histology (worse) vs Tubular
76
Q

What are the familial colon cancer syndromes?

A

HNPCC - over 50% develop cancer

FAP - APC Gene - 100% risk of developing cancer
Multiple polyps form during teenage years
More associated with carcinoid syndrome

Peutz-Jeghers syndrome - STK11 gene - pigmented spots on lips and buccal mucosa

77
Q

What is the oncogene involved in colorectal cancer?

A

K-Ras

78
Q

What tumour marker would you ask for in CRC?

A

Carcinoembryonic antigen (CEA)

79
Q

What investigations would you perform in suspected CRC?

A

Colonic examination - colonoscopy + biopsy is gold-standard

Bloods

CT (abdomen, chest, pelvis) scan to stage

80
Q

What are the treatments for CRC?

A

Tumour resection +/- end-to-end anastamosis of bowel +/- colostomy
Post-op Chemotherapy

81
Q

What is the screening program for CRC?

A

All individuals between 60-74 are invited for faecal occult blood tests (FOB) every 2 years. If positive, then colonoscopy.

High-risk individuals are screened using colonoscopy prior to the age of 45 (first-degree relatives with colon cancer or those from families with family colon cancer syndromes)

82
Q

What is the difference between osmotic and secretory diarrhoea?

A

Osmotic - hypertonic substances in the bowel lumen draw fluid into the intestine. Stops when patient fasts.

Secretory - active intestinal secretion of fluids and electrolytes. Continues when patient fasts.

83
Q

What are the causes of Osmotic diarrhoea?

A

Ingestion of non-absorbable substance (a laxative)

Generalised or a specific malabsorption defect

84
Q

What are the causes of secretory diarrhoea?

A

Enterotoxins
Hormone-secreting tumours
Bile salts
Fatty acids

85
Q

What is organic vs functional diarrhoea?

A

Organic is higher stool weights where as functional is usually increased frequency of stools but smaller volumes.

86
Q

What points towards an organic cause of diarrhoea?

A

Large volumes, nocturnal diarrhoea, bloody stools, weight loss, steatorrhoea

87
Q

How would you investigate chronic diarrhoea? ( >14days)

A

Stool cultures
Baseline bloods - FBC, ESR, coeliac serology,

If watery +/- blood = colonoscopy
If steatorrhoea / abnormal bloods = SBFT or OGD or CT

88
Q

What symptoms suggest a functional GI disorder?

A 
Nausea alone
Vomiting alone
Belching
Post-prandial fullness
Abdominal bloating
Chest pain unrelated to exercise
Urgency first thing in the morning
89
Q

How to treat functional oesophageal disorders?

A

Amitryptalline or Citalopram

90
Q

How to treat functional dyspepsia?

A

Reassurance and lifestyle changes

91
Q

How to investigate IBS?

A

If young, check for coeliac and IBD

If old, colonoscopy and further investigations

92
Q

Name some causes of intestinal obstruction

A 
Adhesions
Hernia's
Crohn's disease
Intussusception
Carcinoma 
Diverticular disease
Volvulus
93
Q

What are the signs of peritonitis?

A

Tender abdomen
Guarding
Rigid abdomen
Absent bowel sounds IF generalised peritonitis

94
Q

What causes appendicitis?

A

A faecolith that obstructs the lumen of the appendix

95
Q

What are the feature of appendicitis?

A

Central abdominal pain, then localises to RIF
Anorexia
D+V
Pyrexia
Tenderness and guarding in RIF (localised peritonitis)

Rovsing’s sign - LIF hurts when you press RIF

96
Q

What investigations would you order for suspected appendicitis?

A

WCC, CRP, ESR are raised
USS may show inflammation and mass
CT is highly sensitive and specific but only used if diagnosis in unclear

97
Q

What is the management of appendicitis?

A

IV Fluids and Abx (Met + Cef)

Surgery

98
Q

What defect results in generalised peritonitis?

A

Rupture of an abdominal viscus results in generalised tenderness over the abdomen as opposed to localised peritonitis.

Pt is shocked, lies still. Check amylase and CXR.

Eg. peforated ulcer, perforated appendix

99
Q

What are the 2 types of intestinal obstruction?

A

Mechanical - dilated bowel above the obstruction. Colicky abdominal pain, vommiting, absolute consitpation, tinkling bowel sounds,
Small bowel = conservative, large bowel = surgical

Functional - paralytic ileus associated with post-op, opiate treatments. Pain often not present and bowel sounds only reduced. Gas is seen throughout bowel in AXR.

100
Q

Name some methods of enteral nutrition

A

Oral
NG Tube - short term
PEG - those who need for more than 2 weeks
Percutaenous Jejunostomy

101
Q

When do patients need nutritional support?

A

BMI < 15 = Severely malnourished

BMI 15-19 = If they are unlikely to eat for next 3-5 days due to their condition

BMI normal = If not expected to eat for next 7-10 days

102
Q

What are the complications of Total Parenteral Nutrition?

A

Catheter related - sepsis, thrombosis, embolism, pneumothorax
Metabolic - hyperglycaemia, hypercalcaemia
Electrolyte disturbance
Liver dysfunction

103
Q

How is TPN given?

A

Catheter - can be central vein or peripheral, only ever used for nutrition, not for drugs

104
Q

What is refeeding syndrome?

A

Can occur within the first few days of refeeding by oral/enteral or parenteral route

Hypophosphatemia, Hypomagnesaemia, Hypokalaemia
Thiamine deficiency

Muscle weakness, rhabdomyolysis, cardiac failure, coma, hallucinations, fits

RFs are anorexia nervosa, alcoholics, rapid weight loss - even if obese.

Treat with Pabrinex (Vitamin supplements) + Feeding + correct electrolyte imbalances

105
Q

How does Orlistat work?

A

Used in obesity occasionally

Inhibits pancreatic lipase

106
Q

When is surgery offered for obesity?

A 
Morbidly obese (BMI > 40) 
Severely obese (BMI > 35) with many complications due to obesity

Treat with Roux-en-Y or or Gastric banding

107
Q

What are the types of antacids?

A

Aluminium Hydroxide - tend to cause constipation
Magnesium mixture - tend to be a laxative
Alginate-containing antacids (Gaviscon)

108
Q

What are Ranitidine and Cimetidine?

A

H2-receptor antagonists

Reduce gastric acid secretions by blocking receptors

Used in GORD, Peptic ulcers, preventing NSAID gastric damage

109
Q

What are the types of laxatives?

A

Bulk-forming - absorb water and increase faecal mass
Used in pts with colostomy, diverticular disease, IBS
Husk, Methylcellulose, Sterculia

Stimulants - increase colonic activity
Used for short term issues
Bisacodyl, Glycerol (Senna)

Osmotic - retain/attract water in the intestinal lumen
Used in treating hepatic encephalopathy
Lactulose, Macrogol, Magnesium or Phophate salts

110
Q

What is Loperamide?

A

Anti-motility agent

Used in UC, Infective diarrhoea,

111
Q

What are most cases of Diarrhoea treated with?

A

Diarolyte which is an oral rehydration salt

112
Q

What are the types of drugs used to treat nausea and vomiting?

A

Antihistamines - block H1 receptors - Cyclizine, Promethazine - used in motion sickness, drug induced vomiting, vertigo

Phenothiazines - Dopamine antagonists - Chlorpromazine - Used for neoplastic disease, radiation sickness, general anaesthetic

Domperidone and Metaclopromide - block dopamine receptors and inhibit dopaminergic stimulation of CRT - used in post-op N+V

5-HT3-receptor antagonists - Block 5-HT3 in the chemoreceptor therapy zone (CRT) in the 4th ventricle - Ondensatron - Used after chemotherapy

Electrolyte Disorders (6 decks)

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